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Article

Comprehensive Dose–Response Analysis of the Effect of Ionizing Radiation on Hepatic Enzyme Parameters in a Rabbit Model

by
Aliyu Yakubu
1,
Ibrahim Abdulazeez Okene
2,3,
Chinedu Amaeze Frank
1,
Maruf Lawal
4,
Shamsaldeen Ibrahim Saeed
1,* and
Mohammed Dauda Goni
1,5,*
1
Public Health and Zoonotic Disease Research Group, Department of Preclinical Sciences, Faculty of Veterinary Medicine, Universiti Malaysia Kelantan, Kota Bharu 16100, Malaysia
2
Veterinary Program, Faculty of Health Sciences, Higher Colleges of Technology, Men Campus, Sharjah 26666, United Arab Emirates
3
Department of Veterinary Surgery and Radiology, University of Maiduguri, Maiduguri 600244, Nigeria
4
Department of Radiology and Surgery, Faculty of Veterinary Medicine, Ahmadu Bello University, Zaria 810211, Nigeria
5
Institute for Artificial Intelligence and Big Data, Universiti Malaysia Kelantan, Kota Bharu 16100, Malaysia
*
Authors to whom correspondence should be addressed.
Radiation 2025, 5(4), 27; https://doi.org/10.3390/radiation5040027
Submission received: 14 August 2025 / Revised: 18 September 2025 / Accepted: 19 September 2025 / Published: 23 September 2025
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Simple Summary

Exposure to radiation can damage the body’s organs, particularly the liver. This study measured the blood levels of three liver enzymes (AST, ALT, and ALP) to examine the effects of varying ionising radiation levels on rabbit liver function. The liver enzyme levels of rabbits exposed to different radiation dosages were monitored over time. The findings indicated that these enzymes significantly increased in response to increasing radiation doses, indicating liver injury or stress. This study advances our knowledge of how radiation impacts the liver and could help establish safe radiation exposure thresholds.

Abstract

Exposure to ionising radiation may be hazardous to living beings, including humans. Ionising radiation exposure has been shown to cause hepatic dysfunction or even liver cancer in persons receiving radiation therapy who do not have liver disease. Changes in hepatic enzyme values may suggest radiation-induced stress on liver cells. Then this experimental study examined the effect of different doses of radiation on the liver enzymes aspartate aminotransferase (AST), alkaline phosphatase (ALP), and alanine aminotransferase (ALT). Methods: Six equal groups of thirty-six New Zealand white rabbits weighing 3 and 5 kg each were formed. The rabbits received total body radiation doses of 0 Gy (Control group), 0.053 Gy, 0.11 Gy, 0.21 Gy, 0.42 Gy, and 0.84 Gy on days, 1, 3, and 5 and week 1, week 2, week 3, and week 4. Generalised Linear Mixed Models (GLMMs) were used to compare the data statistically. Results: There was a significant rise in the serum liver enzyme levels; aspartate aminotransferase (AST), alkaline phosphatase (ALP), and alanine aminotransferase (ALT) all showed a statistically significant time effect after the application of different radiation doses. Based on the group effect of radiation, AST and ALP, but not ALT, showed statistically significant findings.

1. Introduction

Ionising radiation has naturally existed in the surroundings since the Earth existed, and every day, people are exposed to radiation from both man-made and natural sources [1]. Natural radiation originates from numerous sources, with more than sixty naturally occurring radioactive elements found in soil, water, and air. Natural radiation comes mostly from radon, a naturally occurring gas that comes from rock and soil [1]. People regularly breathe in and consume radioactive materials from food, water, and the air. The effects of ionising radiation on living cells are proportionate to the dose absorbed. The biological effects of ionising radiation are greatly determined by several factors, such as radiation type and dose, exposed species and tissue, or age at the period of exposure [2]. Ionising radiation is commonly utilised in veterinary medicine to diagnose and treat a variety of diseases [3,4]. Radiographs, computed tomography, fluoroscopy, and nuclear medicine are the principal techniques that use ionising radiation in veterinary medicine. Internal radiography components are found in the majority of general clinics and speciality referral facilities, making radiography the most often utilised and widely available modality [3]. Radiation has various benefits for humanity. Owing to its extensive recognition, it is currently used in business, academic institutions, health care management, and also in military activities [5]. The liver is a vital organ that is involved in many physiological processes, including the synthesis of plasma proteins, the formation of bile, lipid metabolism, glycometabolism, and the removal of different waste products [6]. Alkaline phosphatase (ALP), aspartate transaminase (AST), and alanine transaminase (ALT) are very important indicators of liver function [7]. Alterations in these enzyme levels can be used to measure the amount of hepatic pressure and possible impairment caused by radiation. The incidence of liver injury was assessed clinically based on the evaluation of alanine aminotransferase (ALT) and aspartate transaminase (AST) levels [8]. One of the most significant groups exposed to ionising radiation is industrial radiographers, whose numbers have rapidly expanded in recent years due to advancements in science and technology [8]. Ionising radiation exposure has been shown to have biological impacts on human health [9], with radiation having both early and late effects on healthy tissues and organs [9,10,11]. Ionising radiation exposure has been shown to cause hepatic dysfunction or even liver cancer in persons receiving radiation therapy who do not have liver disease [12,13,14,15]. Data from cohorts of survivors of the atomic bomb reveal that radiation exposure increased the prevalence of liver cirrhosis [16,17,18], hepatitis B, and hepatitis C infection [18]. Acute high-dose radiation (>10 Gy) can result in substantial liver structural damage and hepatic toxicity according to a number of studies [19,20]. A single dose of 6 Gy gamma radiation administered systemically to rats in an experiment was shown to significantly increase the level of alanine aminotransferase (ALT) and aspartate transaminase (AST) [21,22]. According to an epidemiological study on radiation therapy for cancer in children and adolescents, low hepatotoxicity may result from liver radiation (mean liver dose = 5 Gy) [23]. According to the aforementioned studies, ionising radiation exposure at high doses can cause liver damage. Nonetheless, the majority of nations have adopted the International Commission on Radiological Protection (ICRP)’s recommendation that the yearly effective dose limits for radiation workers should not exceed 20 mSv [24,25]. It is unclear how long-term exposure to this low external dosage of ionising radiation affects liver damage. The liver is regarded as an organ that is vulnerable to radiation according to research [23,26]. Low-dose radiation exposure (single dose between 0.02 and 1.0 Gy) has been shown in animal experiments to promote liver inflammation [27]. This shows that low-dose radiation exposure may have a deleterious effect on liver function and lead to the development of liver disease [8]. Acute ionising radiation exposure can lead to major health problems in vertebrates [28]. Some studies have reported that radiation-induced damage in animal models, including mice and non-human primates (NHPs), is similar to that seen in humans [29,30,31]. Ref. [32] revealed that radiation exposure transformed the levels of hepatic enzymes, indicating probable liver damage. We can contribute to gaining a good understanding of the physiological repercussions of exposure to radiation and its possible health implications by revealing the influence of radiation on hepatic enzymes. This study’s findings are applicable to a number of circumstances, such as workplace exposures, medical radiation therapy, and preparedness for unintentional nuclear disasters. A detailed examination of the effects of radiation on hepatic enzyme parameters will be helpful to health care professionals, policymakers, and emergency personnel.

2. Materials and Methods

2.1. Animals and Management

Thirty-six (36) healthy New Zealand white rabbits (Oryctolagus cuniculus), weighing 3–5 kg, were procured for this experimental study from Lylead Agro Businesses in Jamaa, Kaduna State. The animals were kept in the animal house of the Faculty of Veterinary Medicine, Ahmadu Bello University, Zaria, in cages that were locally constructed. Before the trial began, the rabbits were given two weeks to become used to their new environment, and food and drink were given as needed.

2.2. Experimental Design

The goal of this study was to examine how radiation exposure affected hepatic parameters in a rabbit model. For this investigation, a total of 36 mature New Zealand white rabbits weighing between 3 and 5 kg were employed. The rabbits were divided into a total of six groups at random using a completely randomised design (CRD) experimental model. Only the rabbits that met the inclusion criteria were enrolled in the study, which included healthy rabbits that weighed up to 3 kg or above. For easy identification, all the rabbits were marked with a permanent marker [33]. Prior to the trial, the rabbits were given two weeks to adjust to their new surroundings while receiving food and water as needed. The test subjects were divided into six groups at random: control (n = 6); 0 Gy radiation exposure; 0.053 Gy radiation exposure (n = 6); 0.11 Gy radiation exposure (n = 6); 0.21 Gy radiation exposure (n = 6); 0.42 Gy radiation exposure (n = 6); and 0.84 Gy radiation exposure (n = 6). A geometry progressive model was used for dose selection, which was a square of the preceding doses [34]. Group 1 received 4 exposures, Group 2 received 8 exposures, Group 3 received 16 exposures, while Groups 4 and 5 received 36 and 64 exposures, respectively, at once. This study was carried out in accordance with the guidelines established by the Ahmadu Bello University Animal Care and Use Committee (ABUACUC) and authorised and approved by the Ahmadu Bello University, Zaria, Nigeria, Ethics Committee for Animal Research.

2.3. Radiation Exposure

The rabbits in the radiation exposure groups were subjected to whole-body radiation using a radiation source at a dose rate of 0.0133 Gy/s for the duration of exposure using (MDX-100 Machine, Recorders and Medicare System (P) Ltd., Panchkula, India, www.rmsindia.com (accessed on 4 April 2023). The rabbits were housed in individual cages after exposure for investigation. The whole-body irradiation was carried out in the Radiology Department of the Faculty of Veterinary Medicine in Ahmadu Bello University, Zaria, Nigeria.

2.4. Sample Collection

Prior to irradiation, blood samples were obtained from each rabbit’s ear vein and at 1, 3, 5, 7, 14, 21, and 28 days after irradiation for hepatic enzymes analysis. Blood collected was centrifuged for 15 min at 1500 rpm, and the serum was collected for the analysis. Serum was extracted from blood samples for hepatic enzyme analysis.

2.5. Sample Analysis

Serum was extracted from blood samples following centrifugation at 1500 rpm for 15 min for the hepatic enzyme analysis. The samples were analysed with a semi-automatic biochemistry analyser (Bio 2000, BioPlus SP, Rio De Janeiro, Brazil) using commercial reagents (Labtest diagnosis MG Brazil) according to the manufacturer’s recommendation. Biochemical determinations were carried out after calibration with appropriate calibrators for each liver enzyme (ALT, AST, and ALP) as described earlier by the method used by [35]. Enzyme-specific reagents were produced and placed into the analyser according to the manufacturer’s instructions. Serum samples were put onto the analyser’s sample tray, ensuring that each sample was properly identified and tracked. The analyser pipetted the required amount of serum and mixed it with the appropriate reagent. The reaction between the serum and the reagent resulted in an obvious colour change. The analyser quantified the enzymatic activity in each sample by measuring the absorbance or fluorescence of the reaction products at certain wavelengths. The analyser’s software (the analyser usually work using photometric techniques to measure light absorbance in the samples) recorded and saved the enzyme activity data for each sample. The results were printed, recorded, and expressed in micro litres (μL).

2.6. Statistical Analysis

SPSS software (Version 23.0) was used to analyse the data. To summarise the data, descriptive statistics were utilised and the mean and standard deviation (SD) were used in reporting the findings. We used Generalised Linear Mixed Models (GLMMs) to examine the longitudinal data and account for repeated measures within rabbits. For each haematological parameter, we utilised GLMMs with suitable distributional assumptions and link functions. Radiation dose (as a categorical variable) and time point (as a categorical or continuous variable), as well as their interaction term, were fixed effects in the models. In order to account for the association within rabbits across time points, rabbit ID was introduced as a random intercept. We used covariates in the models to account for any potential confounding variables, such as age and weight. Likelihood ratio tests or information criteria (e.g., AIC or BIC) were used to evaluate model fit and select the best covariance structure. Using appropriate contrasts or pairwise comparisons, post hoc analyses were performed to compare each radiation dose group with the negative control group. The statistical significance level was chosen at p < 0.05. We used GLMMs to account for the linked nature of the repeated measures and to reliably assess the effects of radiation exposure on hepatic parameters while taking within-subject variability and any confounding factors into account. This method will provide robust statistical inference and increase the credibility of our findings.

3. Results

3.1. Aspartate Transaminase (AST)

Table 1 shows a significant mean difference in AST with time: p < 0.001 and partial eta squared: 0.758. The AST reference range is determined for healthy rabbits (14–113 IU/L), and in toxin-induced hepatitis, the level is raised, with the values potentially being much higher than the upper reference range of >200. The post hoc analysis shows that mean AST significantly decreased at day 1 (p = 0.034) and week 1 (p < 0.001) compared to pre-exposure, while mean AST significantly increased at week 3 (p = 0.001) and week 4 compared to pre-exposure. At week 2 (p < 0.001), week 3 (p < 0.001), and week 4 (p < 0.001) mean AST significantly increased compared to day 1. At week 2 (p < 0.001), week 3 (p < 0.001), and week 4 (p = 0.002) mean AST significantly increased compared to day 3. At week 2 (p < 0.001), week 3 (p < 0.001), and week 4 (p = 0.001) mean AST significantly increased compared to day 5. At week 2 (p < 0.001), week 3 (p < 0.001), and week 4 (p = 0.001) mean AST significantly increased compared to week 1.
Based on the group effect, Table 2 shows a significant mean difference in AST between groups: p < 0.001 and partial eta squared: 0.950. The post hoc analysis shows that Groups 1 (p < 0.001), 2 (p = 0.040), 3 (p < 0.001), 4 (p < 0.001), and 5 (p < 0.001) had significantly increased mean AST compared to the control group. Groups 3 (p = 0.001) and 5 (p = 0.001) had significantly increased mean AST compared to Group 1. Groups 3 (p < 0.001) and 5 (p < 0.001) had significantly increased mean AST compared to Group 2.
Table 3 shows the raw values of each dosage group at each time point for AST. The control group retained comparatively constant AST levels with only minor fluctuations, while all treated groups exhibited significant increases, especially from Week 2 onward. Group 1 increased progressively and peaked between weeks 2 and 3; Group 2 fell after a high baseline but recovered strongly before decreasing slightly at week 4; Group 3 remained steadily high with its highest being at week 3; Group 4 declined suddenly after the baseline but then recovered to continue being elevated from week 2 onward; and Group 5 exhibited early variations but the greatest response overall, rising suddenly to a peak of 91 at week 3 before a minor drop. Overall, all treated groups showed a clear AST increase compared to the control, with Group 5 exhibiting the greatest effect.
Based on the interaction effect of exposure to radiation based on time and group, Figure 1 shows a significant interaction between the time effect and the group effect of AST (p < 0.001). In the G0 group, the post hoc analysis shows no significant mean difference in AST (p > 0.0083) between all the time points. In the G1 group, the post hoc analysis shows a significant mean difference in AST (p < 0.0083) between pre-exposure and week 2, week 3, and week 3; day 1 and week 2, week 3, and week 3; day 3 and week 2, week 3, and week 3; day 5 and week 3; and week 1 and week 3. In the G2 group, the post hoc analysis shows a significant mean difference in AST (p < 0.0083) between pre-exposure and week 1; day 1 and week 2 and week 3; day 3 and week 2 and week 3; day 3 and week 2 and week 3; and week 1 and week 2 and week 3. In the G3 group, the post hoc analysis shows a significant mean difference in AST (p < 0.0083) between pre-exposure and week 3; day 1 and week 2, week 3, and week 4; day 3 and week 3; and week 1 and week 3. In the G4 group, the post hoc analysis shows a significant mean difference in AST (p < 0.0083) between pre-exposure and day 1, day 3, day 5, and week 1; day 1 and week 2, week 3, and week 4; day 5 and week 2, week 3, and week 4; day 5 and week 2, week 3, and week 4; and week 1 and week 2, week 3, and week 4. In the G5 group, the post hoc analysis shows a significant mean difference in AST (p < 0.0083) between pre-exposure and week 3 and week 4; day 1 and day 3, day 5, week 2, week 3, and week 4; day 3 and week 2, week 3, and week 4; day 3 and week 2, week 3, and week 4; week 1 and week 3 and week 4; and week 2 and week 3.
This study’s results demonstrate a strong interaction between the time and group effects, with AST levels exhibiting dose-dependent variations following exposure to low-dose X-rays. A principal merit of this work is the explicit delineation of a time-dependent pattern of AST alterations after low-dose X-ray exposure. The notable interaction between time and group effects (p < 0.001) indicates that AST levels were influenced by radiation dosage and the duration after exposure. The initial reduction in AST on day 1 (25.00 U/L), succeeded by a gradual elevation in AST levels on days 5 to 7 (62.33 U/L), indicates that the liver experiences an initial adaptive response, subsequently followed by a secondary stress response, potentially attributable to oxidative damage or inflammation [36]. The delayed elevation in AST seen from day 5 onwards aligns with the findings of [37], who also reported that radiation-induced hepatic injury became more evident following a latency period. This delayed reaction may be due to the gradual buildup of cellular damage, with AST produced from compromised liver cells during the hepatic injury process. Ref. [38] examined the temporal variations in liver enzyme activity post-radiation exposure, observing that substantial enzyme alterations may not manifest immediately but emerge progressively as damage accrues.

3.1.1. Alanine Transaminase (ALT)

To evaluate the effect of radiation exposure at different doses on alanine transaminase (ALT), Table 4 shows a significant mean difference in ALT with time: p < 0.001 and partial eta squared: 0.919. The ALT reference range was found for healthy rabbits (14–80 IU/L), and in toxin-induced hepatitis the level raised with the values, potentially much higher than the upper reference range of >150. The post hoc analysis shows that day 1 (p < 0.001), day 3 (p < 0.001), day 5 (p < 0.001), week 2 (p < 0.001), and week 3 (p < 0.001) mean ALT significantly decreased compared to pre-exposure, while at week 4 (p < 0.001) mean ALT significantly increased compared to pre-exposure. At week 1 (p < 0.001) and week 4 (p < 0.001) mean ALT significantly increased compared to day 1. At week 1 (p < 0.001) and week 4 (p < 0.001) mean ALT significantly increased compared to day 3, while at day 5 (p = 0.001) mean ALT significantly decreased compared to day 3. At week 1 (p < 0.001) and week 4 (p < 0.001) mean ALT significantly increased compared to day 3. At week 2 (p < 0.001) and week 3 (p < 0.001) mean ALT significantly decreased compared to week 1, while at week 4 (p < 0.001) mean ALT significantly increased compared to week 1. At week 4 (p < 0.001) the mean ALT significantly increased compared to week 2. At week 4 (p < 0.001) the mean ALT significantly increased compared to week 3. Table 4 shows no significant mean difference in ALT between groups: p = 0.054 and partial eta squared: 0.557.
Table 5 shows no significant mean difference of ALT between groups, p = 0.054, Partial eta squared 0.557. The table showed the effect of treatment on mean alanine aminotransferase (ALT) levels across the control and five treatment groups. Each group comprised of six animals (N = 6). A mean ALT of 29.69 U/L with a 95% CI ranging from 27.10 to 32.28 was obtained by the control group.In contrast, the treatment groups exhibited slight changes in ALT values: G1 had a mean of 28.50 (95% CI: 25.91–31.09), G2 had the peak mean at 30.31 (95% CI: 27.72–32.90), whereas G3 (25.38; 95% CI: 22.78–27.97) and G5 (25.75; 95% CI: 23.16–28.34) recorded the lowest ALT levels between the treatment groups. G4 revealed a mean ALT of 29.00 (95% CI: 26.41–31.59), which was near to the control group value.
Table 6 shows the raw values of each dosage group at each time point for ALT. The control group exhibited wide fluctuations in ALT with no steady trend, falling sharply after baseline and then rising again to higher values. On the other hand, all treated groups showed noticeable although delayed increases by week 4. Group 1 climbed gradually in the early phase before peaking at 65.5, while Group 2 showed mild fluctuations before a dramatic increase to 62. Group 3 was comparatively stable at lower levels until a noticeable peak at 70, and Group 4 showed the greatest effect, dropping to low levels initially but then rising progressively to reach the peak ALT value of 79.5. Group 5 exhibited lesser fluctuations early on, although concluded with a significant increase to 58. Overall, the findings suggest that while the control values were flexible, all the treatment groups showed distinct late-phase rises in ALT, with Group 4 exhibiting the largest cumulative effect.
The interaction between group and time, as shown in Figure 2, shows that there is a significant interaction between the time effect and the group effect of ALT (p < 0.001). In the G0 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and all-time points, except for week 1: day 1 and day 3, day 5, week 1, and week 4; day 3 and day 5 and week 1; day 5 and week 1, week 2, and week 3; and week 1 and week 2, week 3, and week 4. In the G1 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and week 4; day 1 and week 4; day 3 and day 5 and week 4; day 3 and week 1 and week 4; week 2 and week 4; and week 3 and week 4.
In the G2 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and day 1, day 3, day 5, and week 2; day 1 and week 1, week 3, and week 4; day 3 and week 1, week 3, and week 4; day 5 and week 1, week 3, and week 4; week 1 and week 2; week 2 and week 3; and week 3 and week 4. In the G3 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and week 4; day 1 and week 1 and week 4; day 3 and day 5 and week 4; day 5 and week 4; week 1 and week 4; week 2 and week 4; and week 3 and week 4. In the G4 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and all-time points, except for week 1: day 1 and day 3, day 5, and week 4; day 3 and week 1 and week 4; day 5 and week 1 and week 4; week 1 and week 4; week 2 and week 4; and week 3 and week 4. In the G5 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and week 4; day 1 and week 4; day 3 and day 5 and week 4; day 5 and week 4; week 1 and week 4; week 2 and week 4; and week 3 and week 4.
The analytical findings demonstrated a statistically significant interaction between the time impact and group effect on ALT levels (p < 0.001), demonstrating that ALT levels were affected by radiation dosage and the duration post-exposure. The notable interaction between time and group effect indicates that ALT levels were influenced by both the cumulative X-ray exposure dosage and the duration post-exposure, demonstrating a dynamic interplay between these factors. During this investigation, ALT levels varied during the 7-day observation period; this aligns with other research indicating that liver enzyme activity, especially ALT, may fluctuate over time after radiation exposure [39]. The variations in ALT levels noted in this study may signify the liver’s effort to recuperate or the commencement of a reparative response to sub-lethal damage caused by low-dose radiation. The findings align with research indicating that time and dosage interact to elicit diverse biological responses, including variations in liver enzyme levels [40].

3.1.2. Alkaline Phosphatase (ALP)

Table 7 shows a significant mean difference in ALP with time: p < 0.001 and partial eta squared: 0.708. The ALP reference range is determined for healthy rabbits (10–96 IU/L), and in toxin-induced hepatitis, the level raises with the values, potentially reaching much higher than the upper reference range of >150. The post hoc analysis shows that at day 3 (p < 0.001), day 5 (p = 0.045), week 2 (p = 0.003), week 3 (p = 0.001), and week 4 (p < 0.001) mean ALP significantly increased compared to pre-exposure. At day 3 (p = 0.037), week 2 (p = 0.010), week 3 (p = 0.031), and week 4 (p < 0.001) mean ALP significantly increased compared to day 1, while at week 1 (p = 0.001) mean ALP significantly decreased compared to day 1. At day 5 (p = 0.005) and week 1 (p < 0.001) mean ALP significantly decreased compared to day 2. At week 2 (p < 0.001), week 3 (p < 0.001), and week 4 (p < 0.001) mean ALP significantly decreased compared to week 1.

3.1.3. Group Effect

Table 8 shows a significant mean difference in ALP between groups: p = 0.001 and partial eta squared: 0.778. The post hoc analysis shows that in Groups 1 (p = 0.001), 2 (p = 0.013), and 3 (p = 0.008) the mean ALP significantly increased compared to the control group.
Table 9 shows the raw values of each dosage group at each time point for ALP. The control group exhibited steady ALP levels with very slight fluctuations, while all treatment groups showed rises at various time points. Group 1 exhibited the most consistent elevation, peaking at week 4, while Groups 2 through 4 showed a rise–dip–rise pattern with variations but eventually having higher values than baseline. Group 5 increased quickly and reached its highest value at week 2 then started to decline in week 4. Overall, treatment groups showed varying but generally raised ALP compared to the control group, with Group 1 showing the greatest progressive increase in ALP.

3.1.4. Interaction Effect

Figure 3 shows a significant interaction effect between the time effect and the group effect of ALP (p < 0.001). In the G0 group, the post hoc analysis shows a significant mean difference in ALP (p > 0.0083) between all time points. In the G1 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and week 3 and week 4; day 1 and week 1, week 2, week 3, and week 4; day 3 and week 1, week 3, and week 4; day 5 and week 1, week 3, and week 4; week 1 and week 2, week 3, and week 4; and week 2 and week 3, and week 4. In the G2 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and week 3; day 3 and week 1; week 1 and week 3 and week 4; and week 2 and week 3.
In the G3 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and day 3 and week 4; day 1 and week 1 and week 4; day 3 and day 5 and week 1; day 5 and week 4; week 1 and week 2, week 3, and week 4; and week 2 and week 4. In the G4 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and week 2 and week 4; day 1 and week 1, week 2, and week 4; day 3 and day 5 and week 1; day 5 and week 2 and week 4; week 1 and week 2, week 3, and week 4; and week 2 and week 3. In the G2 group, the post hoc analysis shows a significant mean difference in ALT (p < 0.0083) between pre-exposure and day 3 and week 2; day 1 and week 2; day 3 and week 4; week 1 and week 2; and week 2 and week 3.
The data analysis demonstrated a statistically significant interaction between time and group effects on ALP levels (p < 0.001). This study’s notable interaction between time and group effects on ALP aligns with the investigations that analysed the temporal dynamics of biomarkers post-radiation exposure. Research by [41] indicated that the impact of ionising radiation on ALP activity in rats was non-linear and contingent upon both the radiation dosage and the duration post-exposure. Ref. [42] also noted that the extent of ALP fluctuations in mice subjected to radiation differed at various post-exposure intervals, with certain groups displaying a postponed peak in ALP activity. The temporal variations in ALP activity noted in this study indicate that low-dose radiation elicits a dynamic response in the liver. Similarly to the research conducted by [43], early post-radiation alterations in ALP may signify acute stress responses in hepatocytes. In contrast, subsequent modifications can denote prolonged adaptive or reparative processes. The fluctuations in ALP levels over time indicate that the liver’s reaction to low-dose radiation exposure is not instantaneous, necessitating more research to determine if the rise in ALP is temporary or indicative of sustained hepatic stress.

4. Discussion

Ionising radiation has detrimental effects on living things and is widely used in industry, diagnosis, and therapy, so pharmacological intervention may be the most effective method of protecting humans from ionising radiation or of lessening its harmful effects [44,45]. Animal experiments have demonstrated that ionising radiation exposure causes oxidative stress in a variety of tissues [46,47,48]. The liver is a vital organ that is involved in many physiological processes, including the synthesis of plasma proteins, the formation of bile, lipid metabolism, glycometabolism, and the removal of different waste products [6]. The discoveries of this study shed light on the effects of radiation on hepatic enzyme parameters in a rabbit model. The observed dose-dependent variations in hepatic enzyme levels show that the liver is a radiosensitive organ that is susceptible to acute and chronic radiation injuries [49]. When exposed to radiation, the liver is an organ that is vulnerable to suffer from lipid peroxidation and cell dysfunction, especially at high doses and for long periods of time [50]. Specific liver enzymes, such as ALT, ALP, and AST, exhibited considerable alterations, particularly at higher radiation doses. Changes in hepatic enzyme values may suggest radiation-induced stress on liver cells. The liver is considered the most important organ in the human body; it plays a crucial role in carbohydrate metabolism, bile production, vitamin storage, and hormone secretion. In addition, it is involved in the immune response, blood production, and detoxification [51]. The observed dose-dependent responses highlight the need to consider radiation effects on liver function, particularly in scenarios when humans may be exposed to larger doses, such as in radiation therapy or nuclear events. Ref. [52] discovered that changes in radiation dosage series can cause severe injury in the liver, disrupting both cell structure and function and causing tissue damage and death.
Reactive oxygen species (ROS) are produced when ionising radiation interacts with the biological system [53,54]. ROS causes lipid peroxidation and has a substantial negative impact on the cellular membranes, which produces damage to the cells [55]. The majority of the harm that radiation causes to living things is believed to come from active oxygen species that are created by water and oxygen within the living organism. These reactive oxygen species cause genetic damage and aberrant cell function when they interact with different intracellular components such as DNA, protein, lipids, and carbohydrates. One of the main causes of radiation-induced cellular damage is the production of free radicals and potentially elevated tissue levels of lipid peroxides. According to [56], oxidant-induced damage is thought to be mediated by reactive oxygen species and is linked to an acute-phase response that involves the production of more stress proteins and is mediated by chemokines. Excessive radical production (oxidative stress) can be damaged when there is an imbalance between the generation of free radicals and the defence mechanisms that eliminate them. Because these cellular components are essential to the proper functioning of the cell, lipid peroxidation of biological membranes greatly contributes to the development of radiation-induced cell injury [57]. Exposure to ionising radiation significantly increases the generation of free radicals under oxidative stress [58]. In order to minimise intracellular damage and ensure life under the stressful conditions of irradiation, a sophisticated adaptation of the physiological and biochemical metabolic pathways is needed. Animals with specific antioxidants are expected to have a reduced amount of oxidation in these systems by hydrogen atoms being moved to the structure of free radicals [59]. Excessive generation of free radicals, which occurs in response to many human diseases, environmental stresses, and radiation exposure, is the mediating factor for tissue harm. Reactive oxygen species are minimised and scavenged by antioxidant defence systems found in humans. Nevertheless, these mechanisms are always completely functional during excessive oxidation.
The liver is an exocrine gland that secretes bile into the duodenum via a network of bile ducts. It also functions as an endocrine gland, producing a range of compounds that are discharged into the bloodstream directly [60]. Any harmful substances that enter the liver from the colon or general circulation can be broken down by oxidation or hydroxylation, or detoxified by conjugation, and the byproducts of this breakdown are eliminated in the bile.
Findings from this present study showed that whole body irradiation, delivered as 0 Gy (control group), 0.053 Gy, 0.11 Gy, 0.21 Gy, 0.42 Gy, and 0.84 Gy, induced several alterations in the liver. Concerning the activity of serum liver AST, ALT, and ALP, significant changes were recorded fluctuating between decreased and increased levels up to 0.42 Gy and a highly significant mean increase in AST was recorded in both time and group effects, apart from at day 1 and week 1 that showed a decrease in the mean AST based on time effects. There was also a significant initial decrease in mean ALT based on time effects but it later rose as the dose increased, as seen in week 4, but the group effect showed no significance differences in terms of mean ALT. We also recorded a significant mean increase in ALP serum level both in terms of time and group effects. This fluctuation may be attributed to the decrease in the synthesis of enzymes induced by gamma irradiation, but the accumulation of radiation doses induced highly significant elevations of the serum AST, ALT, and ALP activities as a consequence of irradiation (irreversible reaction), as also detected by [61]. Irradiation causes drastic dysfunction of liver cells, which may lead to increased serum aminotransferase levels. The elevated serum enzymes were also linked to the cellular membrane–gamma ray interaction, leading to an increase in hepatic cell membrane permeability. Furthermore, the increased serum enzymatic activities may also be attributed to the damage of liver parenchymal cells (a hypoxic state) and extrahepatic tissues caused by irradiation, followed by the release of intracellular enzymes into the circulation [62]. In addition, refs. [63,64,65] elucidated that the changes in the enzymatic activities following irradiation may be due either to the release of enzymes from radiosensitive tissues or to alterations in their synthesis.
It has been well documented that both AST and ALT are considered among the most sensitive markers of hepatocellular injury. The registered increase in serum AST and ALT activities in irradiated rabbits in this study is in accordance with the findings of [66]. The last authors attributed the increase in ALT activity in irradiated rats to an extensive breakdown of liver parenchyma with subsequent enzyme release, or to an increase in permeability of the cell membrane that could enhance the movement of enzymes from their sites of production. In contrast, ref. [67] reported a significant decrease in the serum levels of AST, ALT, and ALP following gamma irradiation of rats to different gamma radiation doses compared with the control. They reported that the increase or decrease in the activity of liver enzymes and kidney function parameters might indicate the occurrence of liver and kidney injury. Transaminases play an important role in protein and amino acid metabolism. They are found in the cells of almost all body tissues, and when diseases or injuries affect these tissues, they are released into the bloodstream [68]. One of the proposed mechanisms in this model is considered to be initiated by the accumulation of free radicals, which causes consecutive lipid peroxidation of the cell membranes and endoplasmic reticulum. The alterations in the activity of transaminases brought on by radiation were found to be contradictory. While some authors observed a drop in activity, others noted an increase. The increase in the serum aminotransferase activities could be due to liver damage induced by free radicals generated after radiation exposure [69]. The peroxidative products caused the cell membrane to become leaky, with the consequent release of these enzymes into the blood. This suggestion was supported by the work of [70], who reported that lipid peroxidation is recognised to be a major factor in the liver injury model. Refs. [62,71] suggested that the increase in serum ALT is particular to the drastic physiological effects on the liver caused either by direct interaction of cellular membranes with gamma rays or indirectly through the action of free radicals produced by these reactions. Ref. [72] reported that outflow from the impaired tissue is a basis of normalcy in ALT/AST levels. Raised levels of ALT/AST are used to spot hepatitis, autoimmune diseases, toxicity, and ischemic disorders. Mild elevation levels of AST can be a sign of a liver disease, while moderate levels can be an indication of extrahepatic biliary atresia (EHBA), IHBA (intrahepatic biliary hypoplasia), infiltrating conditions, or granulomatous hepatitis. A study by [73] showed that the level of aspartate transaminase (AST) was significantly increased in response to whole-body γ-irradiation as compared with unirradiated rats. The increase in serum AST levels might be interpreted as a response to oxidative stress or may be a result of lesions arising in liver function following its cellular damage and the subsequent release of the liver’s intracellular enzymes into the bloodstream [74]. The recorded rise might also be due to a hypoxic state in the parenchymal liver cells, and enhanced permeability of the cell membrane [75] or mitochondrial membrane [76] could also be the cause of these observed elevations, resulting in the release of intracellular enzymes into the circulation. The decrease in some enzyme activities (AST) can be attributed to the inactivation of their biosynthesis [77]. Ref. [78] observed a statistically elevated serum level of AST in New Zealand white rabbits following total body irradiation, suggesting that the elevation of this serum biochemistry likely reflects liver injury. Ref. [79] also reported a significant increase in liver enzyme AST following whole-body irradiation; such an increase may be a result of hepatocellular damage caused by exposure to ionising radiation. Ref. [80] reported that rats in the group exposed to whole-body irradiation had substantially higher serum AST activities than the control group in a radioprotective study of the effect of date syrup. It is important to note that the AST serum level rises due to liver and RBC damage, as AST exists in both RBCs and hepatocytes [81]. The elevated serum level of AST recorded in this study reflects injury to the liver. AST has been identified as a valuable biomarker for the prognosis and monitoring of liver damage in numerous investigations [8,82].
The present study suggests that the increase in AST activities might be explained by either a modification in membrane absorptivity or the breakdown of liver cells, as these two factors are indicative of different types of liver disease. Because of their intracellular position within the cytosol, serum aminotransferase enzyme activity was increased [83] as a result of damage to the liver and a subsequent breakdown in the cell membrane architecture, causing the enzymes to leak into the serum, where their concentration rose.
Findings from this study showed a statistically significant decrease based on the effect of ionising radiation on ALT with time, though a later rise was seen with an increased radiation dose at week 4, but there was no significant mean difference based on the effect of ionising radiation on ALT between groups. The increased ALT activities found in our data could be caused by the liver parenchyma breaking down extensively and releasing enzymes as a result, or they could be caused by the cell membrane being more permeable, which would facilitate the flow of enzymes away from the sites of production [66]. Ref. [84] found a significant decrease in the serum levels of the liver enzyme ALT in rats exposed to gamma irradiation in a study evaluating newly created gallium nanoparticles (GaNPs) in combination with low doses of gamma radiation (γR) for therapeutic purposes. Ref. [85] also reported a decreased serum level of ALT in the UV-C HOT-irradiated rabbit group compared to septic rabbits without treatment. Ref. [86] observed no significant changes in serum levels of alanine aminotransferase (ALT) in a high-single-dose-irradiated rat compared with the controls. Ref. [10] reported no statistically significant difference in ALT between controls and radiologic technician (RT) groups in an investigation of the risk factors for liver dysfunction in a selected group of radiologic technicians (RTs) in order to assess the correlation between cumulative radiation exposure and hepatic injury. ALT has been identified as a valuable biomarker for the prognosis and monitoring of liver damage in numerous investigations [8,82]. All the changes or differences we observed in this report compared to the previous findings may be largely due to time or duration of exposure and the radiation dose received, which play a major role in hepatic physiology when exposed to radiation.
Furthermore, the findings of the present study revealed that total body irradiation significantly increased ALP activity in the serum, as also reported by [54]. It is well recognised that ALP plays a significant role in keeping the cell membrane permeable [87]. Radiation exposure triggered impairment to the cell membrane that amplified ALP activity. The rises in ALP activity also might be due to the alterations in the amino acid residues and catalytic action of ALP [88]. Overproduction and outflow in blood are the basis of the anomalies in ALP levels [89]. According to reports, the serum of irradiated rats showed a significant rise (p ≤ 0.05) in ALP activity levels. This increase may have been caused by radiation-induced disruption to cell membranes, which may have led to the release of intracellular molecules into the bloodstream [68]. Ref. [22] reported that rats in the group exposed to whole-body irradiation had substantially higher serum ALP activities than the control group in a radioprotective study of the effect of date syrup. Ref. [86] observed a statistically significant rise in serum levels of alkaline phosphatase (ALP) following high fractionated irradiation of rats compared with the controls. In accordance with the findings of this report, ref. [90] also reported a statistically significant increase in serum levels of ALP during radiotherapy in patients with abdominal and lower thoracic cancer [91]. Another study reported a significant rise in serum levels of ALP in a study of the radioprotective effect of arbutin in megavoltage therapeutic X-irradiated mice. Ref. [92] reported a significant increase in ALP serum levels following gamma irradiation of male Sprague-Dawley rats. According to [93], high levels of the ALP enzyme indicate a liver problem. All the changes or differences we observed in this report compared to the previous findings may be largely due to time or duration of exposure and the radiation dose received, which play a major role in hepatic physiology when exposed to radiation.
Understanding the effect of radiation on hepatic enzyme parameters is critical for determining the potential health concerns associated with radiation exposure, as liver function is critical for overall physiological balance. More research is needed to determine the particular processes behind these alterations in hepatic enzymes and to investigate techniques for minimising radiation-induced effects on liver function.

5. Conclusions

Our findings show that radiation doses ranging from 0.053 Gy to 0.84 Gy cause dose-dependent changes in hepatic enzyme parameters in a rabbit model. Biochemically, substantial alterations in liver enzymes such as ALT, AST, and ALP indicate cellular damage and hepatic stress caused by radiation exposure. These enzyme markers are essential indicators for measuring the liver’s capacity to metabolise and detoxify, stressing the negative effects of long-term radiation exposure on the organ. These discoveries help improve our understanding of how radiation affects liver function. Future research should concentrate on elucidating the underlying mechanisms and devising strategies to reduce the likelihood of unfavourable outcomes in radiation-exposed individuals.

Author Contributions

This research was carried out with contributions from all authors. Conceptualization and methodology: A.Y. and I.A.O.; M.D.G. analysed and interpreted the data; I.A.O., S.I.S. and A.Y. conducted writing of the manuscript and revision; C.A.F. and M.L. were involved in data collection and manuscript review. The final draft of the manuscript was read, critically reviewed, and approved by all authors. All authors have read and agreed to the published version of the manuscript.

Funding

This research received no external funding.

Institutional Review Board Statement

This research was carried out in accordance with the recommendations of the Animal Care and Use Committee at Ahmadu Bello University Zaria, Nigeria, on the 31 January 2022. The experimental procedures were also approved by the Animal Care and Use Committee (ABUCAUC) at Ahmadu Bello University Zaria with approval number (ABUCAUC/2022/014).

Informed Consent Statement

Not applicable.

Data Availability Statement

The manuscript contains the datasets and all pertinent information used in this research.

Acknowledgments

The authors are grateful for the contributions of members of the faculty of Veterinary Medicine Ahmadu Bello University Zaria; the staff of the Surgery and Radiology department of Ahmadu University Zaria; and the Staff of the faculty of Veterinary Medicine University of Malaysia Kelantan.

Conflicts of Interest

The authors have disclosed no competing interests.

Abbreviations

The following abbreviations are used in this manuscript:
ABUACUCAhmadu Bello University Animal Care and Use Committee
AICAkaike Information Criterion
ALTAlanine Aminotransferase
ALPAlkaline Phosphatase
ASTAspartate Aminotransferase
BICBayesian Information Criterion
CIConfidence Interval
DFDegree of Freedom
EHBAExtrahepatic Biliary Atresia
GaNPsGallium Nanoparticles
γRGamma Radiation
GLMMsGeneralised Linear Mixed Models
GyGray
IHBAIntrahepatic Biliary Hypoplasia
RTsRadiologic Technicians
SDStandard Deviation
SPSSStatistical Software for the Social Sciences

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Figure 1. Time and group interactions of AST.
Figure 1. Time and group interactions of AST.
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Figure 2. Time and group interactions of ALT.
Figure 2. Time and group interactions of ALT.
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Figure 3. Time and group interactions of ALP.
Figure 3. Time and group interactions of ALP.
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Table 1. The effect of time on mean AST.
Table 1. The effect of time on mean AST.
TimeNMean (95% CI)F (DF)pPartial Eta Squared
Pre-exposure 642.33 (37.72, 46.95)37.50 (7, 84)<0.0010.758
Day 1625.00 (20.53, 29.47)
Day 3628.75 (22.05, 35.46)
Day 5630.83 (24.13, 37.54)
Week 1632.42 (27.85, 37.00)
Week 2654.75 (51.58, 57.92)
Week 3662.33 (58.67, 66.00)
Week 4655.92 (51.00, 60.83)
CI = confidence interval, DF = degree of freedom, N = number of animals in each group.
Table 2. The effect of the treatment group on the mean AST.
Table 2. The effect of the treatment group on the mean AST.
GroupNMean (95% CI)F (DF)pPartial Eta Squared
Control623.69 (20.18, 27.19)45.95 (5, 12)<0.0010.950
G1638.75 (35.24, 42.26)
G2637.13 (33.62, 40.63)
G3652.56 (49.06, 56.07)
G4644.75 (41.24, 48.26)
G5652.38 (48.87, 55.88)
G = group, CI = confidence interval, DF = degree of freedom, N = number of animals in each group.
Table 3. AST raw values of each dosage group at each time point.
Table 3. AST raw values of each dosage group at each time point.
PRE-EXPODay 1Day 3Day 5Week 1Week 2Week 3Week 4
C23.5 ± 3.7518 ± 3.4622.5 ± 3.7527 ± 0.5816.5 ± 0.8726.5 ± 2.6027.5 ± 4.3328 ± 3.46
G123.5 ± 3.1828 ± 1.1524 ± 2.3130.5 ± 1.4431.5 ± 1.4454.5 ± 3.1859.5 ± 3.7558.5 ± 1.44
G249.5 ± 3.1822.5 ± 2.0224 ± 1.7327.5 ± 2.0222.5 ± 2.0253.5 ± 3.1859 ± 2.8938.5 ± 6.64
G343 ± 10.9740 ± 11.5545 ± 13.2848.5 ± 17.0347.5 ± 11.2662.5 ± 2.0269.5 ± 0.2964.5 ±3.75
G471 ± 1.7323.5 ± 0.8718.5 ± 1.4418 ± 0.5832 ± 4.6265.5 ± 6.6467.5 ± 7.2262 ± 1.73
G543.5 ± 2.0218 ± 038.5 ± 11.8433.5 ± 6.6444.5 ± 2.0266 ± 1.1591 ± 2.8984 ± 10.39
± = Mean standard deviation.
Table 4. The effect of time on mean ALT.
Table 4. The effect of time on mean ALT.
TimeNMean (95% CI)F (DF)pPartial Eta Squared
Pre-exposure 634.50 (30.82, 38.18)137.02 (7, 84)<0.0010.919
Day 1617.92 (16.29, 19.54)
Day 3619.17 (17.47, 20.86)
Day 5616.17 (14.43, 17.91)
Week 1637.25 (33.13, 41.37)
Week 2619.67 (16.70, 22.63)
Week 3619.42 (18.20, 20.64)
Week 4660.75 (56.61, 64.89)
CI = confidence interval, DF = degree of freedom, N = number of animals in each group.
Table 5. The effect of the treatment group on the mean ALT.
Table 5. The effect of the treatment group on the mean ALT.
GroupNMean (95% CI)F (DF)pPartial Eta Squared
Control629.69 (27.10, 32.28)3.02 (5, 12)0.0540.557
G1628.50 (25.91, 31.09)
G2630.31 (27.72, 32.90)
G3625.38 (22.78, 27.97)
G4629.00 (26.41, 31.59)
G5625.75 (23.16, 28.34)
G = group, CI = confidence interval, DF = degree of freedom, N= number of animals in each group.
Table 6. ALT raw values of each dosage group at each time point.
Table 6. ALT raw values of each dosage group at each time point.
PRE-EXPODay 1Day 3Day 5Week 1Week 2Week 3Week 4
C60 ± 3.4614 ± 2.3121 ± 1.7328.5 ± 1.4459 ± 1.7313 ± 2.3112.5 ± 1.4429.5 ± 7.22
G120.5 ± 3.1825 ± 2.8927 ± 1.7314.5 ± 0.2933 ± 4.0422.5 ± 4.3320 ± 1.1565.5 ± 3.75
G241 ± 0.5819.5 ± 0.8718 ± 1.1516.5 ± 0.8738.5 ± 3.7518.5± 0.2928.5 ± 1.4462 ± 2.31
G322 ± 2.3113 ± 1.1518.5 ± 2.0214.5 ± 2.6029.5 ± 5.4820.5 ± 0.2915 ± 1.1570 ± 1.15
G438.5 ± 4.3320 ± 1.7313.5 ± 1.4410 ± 1.1533.5 ± 0.2918 ± 6.3519 ± 0.5879.5 ± 4.91
G525 ± 7.5116 ± 1.1517 ± 2.8913 ± 3.4630 ± 8.0825.5 ± 1.4421.5 ± 2.0258 ± 5.77
± = Mean, standard deviation.
Table 7. The effect of time on mean ALP.
Table 7. The effect of time on mean ALP.
TimeNMean (95% CI)F (DF)pPartial Eta Squared
Pre-exposure611.83 (9.65, 14.02)29.15 (7, 84)<0.0010.708
Day 1616.08 (14.42, 17.74)
Day 3620.17 (18.71, 21.62)
Day 5616.08 (14.27, 17.90)
Week 1610.50 (8.90, 12.10)
Week 2620.83 (19.05, 22.62)
Week 3621.67 (19.86, 23.47)
Week 4621.17 (19.98, 22.35)
CI = confidence interval, DF = degree of freedom, N = number of animals in each group.
Table 8. The effect of the treatment group on the mean ALP.
Table 8. The effect of the treatment group on the mean ALP.
GroupNMean (95% CI)F (DF)pPartial Eta Squared
Control614.75 (13.67, 15.83)8.39 (5, 12)0.0010.778
G1619.00 (17.92, 20.08)
G2617.81 (16.74, 18.89)
G3618.00 (16.92, 19.08)
G4617.00 (15.92, 18.08)
G5617.19 (16.11, 18.27)
G = group, CI = confidence interval, DF = degree of freedom, N = number of animals in each group.
Table 9. ALP raw values of each dosage group at each time point.
Table 9. ALP raw values of each dosage group at each time point.
PRE-EXPODay 1Day 3Day 5Week 1Week 2Week 3Week 4
C11 ± 0.5816.5 ± 1.4415 ± 1.7319 ± 0.5815 ± 2.8912 ± 016 ± 3.4613.5 ± 1.44
G111.5 ± 3.7514 ± 1.1519.5 ± 0.8718 ± 0.586.5 ± 1.4422 ± 0.5829.5 ± 0.8731 ± 0.58
G214 ± 0.5816.5 ± 3.1820.5 ± 0.8717.5 ± 1.4411 ± 2.3117 ± 1.1526.5 ± 2.6019.5 ± 0.87
G311 ± 4.0419 ± 0.5824 ± 2.3112 ± 1.159.5 ± 1.4421 ± 1.7321 ± 1.7326.5 ± 1.44
G411.5 ± 1.4416 ± 1.7320.5 ± 2.0213.5 ± 4.336 ± 0.5826.5 ± 4.3318.5 ± 1.4423.5 ± 2.02
G512 ± 1.7314.5 ± 2.0221.5 ± 1.4416.5 ± 1.4415 ± 1.1526.5 ± 0.8718.5 ± 0.2913 ± 1.15
± = Mean (standard deviation).
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Yakubu, A.; Abdulazeez Okene, I.; Frank, C.A.; Lawal, M.; Saeed, S.I.; Goni, M.D. Comprehensive Dose–Response Analysis of the Effect of Ionizing Radiation on Hepatic Enzyme Parameters in a Rabbit Model. Radiation 2025, 5, 27. https://doi.org/10.3390/radiation5040027

AMA Style

Yakubu A, Abdulazeez Okene I, Frank CA, Lawal M, Saeed SI, Goni MD. Comprehensive Dose–Response Analysis of the Effect of Ionizing Radiation on Hepatic Enzyme Parameters in a Rabbit Model. Radiation. 2025; 5(4):27. https://doi.org/10.3390/radiation5040027

Chicago/Turabian Style

Yakubu, Aliyu, Ibrahim Abdulazeez Okene, Chinedu Amaeze Frank, Maruf Lawal, Shamsaldeen Ibrahim Saeed, and Mohammed Dauda Goni. 2025. "Comprehensive Dose–Response Analysis of the Effect of Ionizing Radiation on Hepatic Enzyme Parameters in a Rabbit Model" Radiation 5, no. 4: 27. https://doi.org/10.3390/radiation5040027

APA Style

Yakubu, A., Abdulazeez Okene, I., Frank, C. A., Lawal, M., Saeed, S. I., & Goni, M. D. (2025). Comprehensive Dose–Response Analysis of the Effect of Ionizing Radiation on Hepatic Enzyme Parameters in a Rabbit Model. Radiation, 5(4), 27. https://doi.org/10.3390/radiation5040027

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