Search Results (15)

Yellow stunt and root rot causes premature degradation of Astragalus adsurgens grasslands in China. However, the etiological factors underlying livestock poisoning following the ingestion of diseased plants remain elusive. The present study aimed to comprehensively characterize the alterations in toxic substances such as swainsonine and trace element profiles in A. adsurgens after infection with Alternaria gansuense, thereby elucidating the underlying mechanisms of livestock toxicity. Using ELISA and regression analyses, we found that diseased plants had higher selenium levels than the healthy ones, with varietal differences. Selenium in the Zahua variety was higher in healthy plants, while diseased plants of the Henan variety had the highest levels. Moreover, the diseased plants demonstrated decreased levels of iron, zinc, sodium, and magnesium, while manganese and calcium concentrations remained unchanged. Swainsonine was detected in both the healthy and infected specimens of Zhongsha No.1 and Henan varieties, with a marked post-infection increase. In conclusion, swainsonine is the primary toxin causing livestock poisoning, and it is unlikely that soil-accumulated selenium poisons animals. However, potential correlations might exist among the contents of selenium, sodium, and swainsonine. We recommend the cautious use of diseased A. adsurgens as livestock feed. Full article

Background: Manganese (Mn) is an essential trace element for humans. It has been recognized as a potential occupational toxin, but its danger as a toxin in patients under parenteral nutrition is often forgotten. Case Presentation: A 73-year-old man was logged for 210 days in the intensive care unit (ICU), receiving parenteral nutrition (PN) for a month, and was then transferred, first, to the internal medicine ward and, then, to the rehabilitation hospital, and 223 days after discharge from the ICU, he had current disease, chorea-type movements in the head and neck, and left hemibody. Diagnostic tests: The magnetic resonance imaging findings suggested manganese deposits, with a total blood manganese concentration of 34 µg·L⁻¹ (reference range: less than 13 µg·L⁻¹). Discussion: Abnormal movements can be caused by manganese poisoning due to parenteral nutrition and are associated with liver failure in the ICU. Our patient showed toxic Mn concentrations in whole blood after 31 days of receiving 300 μg·d⁻¹ of Mn in PN, a shorter duration than typically reported. Neurotoxicity was observed several months later (223 days). Factors such as liver dysfunction and iron deficiency can modulate neurotoxicity. Age may also be a susceptibility factor due to increased expression of Mn transport proteins. Magnetic resonance imaging (MRI) intensity in the globus pallidus is useful for detecting brain Mn accumulation, but it is not feasible for routine clinical practice. Conclusions: In this case, choreiform movements were attributed to manganese (Mn) accumulation in the basal ganglia. It is essential to monitor patients receiving parenteral nutrition (PN) solutions containing Mn, especially in those who have biomarkers of susceptibility, even if they have not yet shown neurological signs, and routinely measure whole-blood Mn concentrations, iron levels, age, and liver function. If Mn intoxication is suspected, a brain MRI examination should be conducted. Full article

A field experiment with winter wheat (Triticum aestivum L.) cultivation was conducted at the Research and Education Centre in Tomaszkowo, Poland (53°72′ N; 20°42′ E) in the years 2013–2016. Fertilisation with nitrogen at 150 and 200 kg ha⁻¹ and foliar application of manganese at 0.5 and 1.5 kg ha⁻¹ were the research factors. Wheat infestation by Fusarium spp. was determined by the habitat conditions during crop growth. Neither nitrogen nor manganese fertilisation affected the presence of Fusarium spp. symptoms on wheat ears, but the infestation intensity decreased with increasing nitrogen and manganese content in the grain. Only the level of deoxynivalenol (DON) was correlated with Fusarium spp. infestation. Increasing the nitrogen fertilisation rate from 150 kg ha⁻¹ to 200 kg ha⁻¹ resulted in higher grain contamination with toxins. Supplementation of nitrogen fertilisation with manganese reduced the number of mycotoxins in wheat grain. The grain yield was mainly affected by the varied weather conditions during the wheat-growing periods. Neither nitrogen nor manganese fertilisation differentiated the wheat grain yield. The objective of this study was to examine the impact of the weather conditions and nitrogen and manganese fertilisation on the grain yield, occurrence of Fusarium head blight and mycotoxin level in winter wheat grain. Full article

Mitochondria play a crucial role in cellular respiration, ATP production, and the regulation of various cellular processes. Mitochondrial dysfunctions have been directly linked to pathophysiological conditions, making them a significant target of interest in toxicological research. In recent years, there has been a growing need to understand the intricate effects of xenobiotics on human health, necessitating the use of effective scientific research tools. Caenorhabditis elegans (C. elegans), a nonpathogenic nematode, has emerged as a powerful tool for investigating toxic mechanisms and mitochondrial dysfunction. With remarkable genetic homology to mammals, C. elegans has been used in studies to elucidate the impact of contaminants and drugs on mitochondrial function. This review focuses on the effects of several toxic metals and metalloids, drugs of abuse and pesticides on mitochondria, highlighting the utility of C. elegans as a model organism to investigate mitochondrial dysfunction induced by xenobiotics. Mitochondrial structure, function, and dynamics are discussed, emphasizing their essential role in cellular viability and the regulation of processes such as autophagy, apoptosis, and calcium homeostasis. Additionally, specific toxins and toxicants, such as arsenic, cadmium, and manganese are examined in the context of their impact on mitochondrial function and the utility of C. elegans in elucidating the underlying mechanisms. Furthermore, we demonstrate the utilization of C. elegans as an experimental model providing a promising platform for investigating the intricate relationships between xenobiotics and mitochondrial dysfunction. This knowledge could contribute to the development of strategies to mitigate the adverse effects of contaminants and drugs of abuse, ultimately enhancing our understanding of these complex processes and promoting human health. Full article

The VapBC system, which belongs to the type II toxin–antitoxin (TA) system, is the most abundant and widely studied system in Mycobacterium tuberculosis. The VapB antitoxin suppresses the activity of the VapC toxin through a stable protein–protein complex. However, under environmental stress, the balance between toxin and antitoxin is disrupted, leading to the release of free toxin and bacteriostatic state. This study introduces the Rv0229c, a putative VapC51 toxin, and aims to provide a better understanding of its discovered function. The structure of the Rv0229c shows a typical PIN-domain protein, exhibiting an β1-α1-α2-β2-α3-α4-β3-α5-α6-β4-α7-β5 topology. The structure-based sequence alignment showed four electronegative residues in the active site of Rv0229c, which is composed of Asp8, Glu42, Asp95, and Asp113. By comparing the active site with existing VapC proteins, we have demonstrated the justification for naming it VapC51 at the molecular level. In an in vitro ribonuclease activity assay, Rv0229c showed ribonuclease activity dependent on the concentration of metal ions such as Mg²⁺ and Mn²⁺. In addition, magnesium was found to have a greater effect on VapC51 activity than manganese. Through these structural and experimental studies, we provide evidence for the functional role of Rv0229c as a VapC51 toxin. Overall, this study aims to enhance our understanding of the VapBC system in M. tuberculosis. Full article

Hepatic encephalopathy (HE) is a neuropsychiatric syndrome derived from metabolic disorders due to various liver failures. Clinically, HE is characterized by hyperammonemia, EEG abnormalities, and different degrees of disturbance in sensory, motor, and cognitive functions. The molecular mechanism of HE has not been fully elucidated, although it is generally accepted that HE occurs under the influence of miscellaneous factors, especially the synergistic effect of toxin accumulation and severe metabolism disturbance. This review summarizes the recently discovered cellular mechanisms involved in the pathogenesis of HE. Among the existing hypotheses, ammonia poisoning and the subsequent oxidative/nitrosative stress remain the mainstream theories, and reducing blood ammonia is thus the main strategy for the treatment of HE. Other pathological mechanisms mainly include manganese toxicity, autophagy inhibition, mitochondrial damage, inflammation, and senescence, proposing new avenues for future therapeutic interventions. Full article

Parkinson’s disease (PD) is a gradually progressing neurodegenerative condition that is marked by a loss of motor coordination along with non-motor features. Although the precise cause of PD has not been determined, the disease condition is mostly associated with the exposure to environmental toxins, such as metals, and their abnormal accumulation in the brain. Heavy metals, such as iron (Fe), mercury (Hg), manganese (Mn), copper (Cu), and lead (Pb), have been linked to PD and contribute to its progression. In addition, the interactions among the components of a metal mixture may result in synergistic toxicity. Numerous epidemiological studies have demonstrated a connection between PD and either single or mixed exposure to these heavy metals, which increase the prevalence of PD. Chronic exposure to heavy metals is related to the activation of proinflammatory cytokines resulting in neuronal loss through neuroinflammation. Similarly, metals disrupt redox homeostasis while inducing free radical production and decreasing antioxidant levels in the substantia nigra. Furthermore, these metals alter molecular processes and result in oxidative stress, DNA damage, mitochondrial dysfunction, and apoptosis, which can potentially trigger dopaminergic neurodegenerative disorders. This review focuses on the roles of Hg, Pb, Mn, Cu, and Fe in the development and progression of PD. Moreover, it explores the plausible roles of heavy metals in neurodegenerative mechanisms that facilitate the development of PD. A better understanding of the mechanisms underlying metal toxicities will enable the establishment of novel therapeutic approaches to prevent or cure PD. Full article

Microcystis aeruginosa is a widespread cyanobacteria capable of producing hepatotoxic microcystins. Understanding the environmental factors that influence its growth and toxin production is essential to managing the negative effects on freshwater systems. Some micronutrients are important cofactors in cyanobacterial proteins and can influence cyanobacterial growth when availability is limited. However, micronutrient requirements are often species specific, and can be influenced by substitution between metals or by luxury uptake. In this study, M. aeruginosa was grown in modified growth media that individually excluded some micronutrients (cobalt, copper, iron, manganese, molybdenum) to assess the effect on growth, toxin production, cell morphology and iron accumulation. M. aeruginosa growth was limited when iron, cobalt and manganese were excluded from the growth media, whereas the exclusion of copper and molybdenum had no effect on growth. Intracellular microcystin-LR concentrations were variable and were at times elevated in treatments undergoing growth limitation by cobalt. Intracellular iron was notably higher in treatments grown in cobalt-deplete media compared to other treatments possibly due to inhibition or competition for transporters, or due to irons role in detoxifying reactive oxygen species (ROS). Full article

Numerous factors affect reproduction, including stress, diet, obesity, the use of stimulants, or exposure to toxins, along with heavy elements (lead, silver, cadmium, uranium, vanadium, mercury, arsenic). Metals, like other xenotoxins, can cause infertility through, e.g., impairment of endocrine function and gametogenesis or excess production of reactive oxygen species (ROS). The advancement of nanotechnology has created another hazard to human safety through exposure to metals in the form of nanomaterials (NMs). Nanoparticles (NPs) exhibit a specific ability to penetrate cell membranes and biological barriers in the human body. These ultra-fine particles (<100 nm) can enter the human body through the respiratory tract, food, skin, injection, or implantation. Once absorbed, NPs are transported to various organs through the blood or lymph. Absorbed NPs, thanks to ultrahigh reactivity compared to bulk materials in microscale size, disrupt the homeostasis of the body as a result of interaction with biological molecules such as DNA, lipids, and proteins; interfering with the functioning of cells, organs, and physiological systems; and leading to severe pathological dysfunctions. Over the past decades, much research has been performed on the reproductive effects of essential trace elements. The research hypothesis that disturbances in the metabolism of trace elements are one of the many causes of infertility has been unquestionably confirmed. This review examines the complex reproductive risks for men regarding the exposure to potentially harmless xenobiotics based on a series of 298 articles over the past 30 years. The research was conducted using PubMed, Web of Science, and Scopus databases searching for papers devoted to in vivo and in vitro studies related to the influence of essential elements (iron, selenium, manganese, cobalt, zinc, copper, and molybdenum) and widely used metallic NPs on male reproduction potential. Full article

The fungal secondary metabolite patulin is a mycotoxin widespread in foods and beverages which poses a serious threat to human health. However, no enzyme was known to be able to degrade this mycotoxin. For the first time, we discovered that a manganese peroxidase (MrMnP) from Moniliophthora roreri can efficiently degrade patulin. The MrMnP gene was cloned into pPICZα(A) and then the recombinant plasmid was transformed into Pichia pastoris X-33. The recombinant strain produced extracellular manganese peroxidase with an activity of up to 3659.5 U/L. The manganese peroxidase MrMnP was able to rapidly degrade patulin, with hydroascladiol appearing as a main degradation product. Five mg/L of pure patulin were completely degraded within 5 h. Moreover, up to 95% of the toxin was eliminated in a simulated patulin-contaminated apple juice after 24 h. Using Escherichia coli as a model, it was demonstrated that the deconstruction of patulin led to detoxification. Collectively, these traits make MrMnP an intriguing candidate useful in enzymatic detoxification of patulin in foods and beverages. Full article

The gut microbiota plays a critical role in chronic kidney disease (CKD) and hypertension. Trimethylamine-N-oxide (TMAO) and trimethylamine (TMA) are gut microbiota-derived metabolites, and both are known uraemic toxins that are implicated in CKD, atherosclerosis, colorectal cancer and cardiovascular risk. Therefore, the detection and quantification of TMAO, which is a metabolite from gut microbes, are important for the diagnosis of diseases such as atherosclerosis, thrombosis and colorectal cancer. In this study, a new “colour-switch” method that is based on the combination of a plasma separation pad/absorption pad and polyallylamine hydrochloride-capped manganese dioxide (PAH@MnO₂) nanozyme was developed for the direct quantitative detection of TMAO in whole blood without blood sample pretreatment. As a proof of concept, a limit of quantitation (LOQ) of less than 6.7 μM for TMAO was obtained with a wide linear quantification range from 15.6 to 500 μM through quantitative analysis, thereby suggesting potential clinical applications in blood TMAO monitoring for CKD patients. Full article

Diarrhetic Shellfish Poisoning (DSP) toxicity was revealed in the Mediterranean blue mussel (Mytilus galloprovincialis) from the Bay of Mali Ston, in the south part of the Eastern Adriatic Sea, through the Croatian National Monitoring Programme in the period from January until June of 2011. A survey of DSP toxicity within the frame of regular controls carried out through the mouse bioassay (MBA, at the time the official method for DSP toxins) demonstrated that in some incidents, positive MBA, which manifested by the atypical symptomatology of the animals, dominated. Additional studies were done to explain the atypical results of the conducted biological tests at the time. In the current study, the bioaccumulated manganese concentration in the soft tissues of mussels was measured to investigate its influence on the MBA results. In both DSP negative and DSP positive samples, which were prepared for the analysis according to the modified US EPA 3052 method, the concentration of the bioaccumulated manganese was performed on the atomic absorption spectrometer using flame atomic absorption spectroscopy technique. The analysis revealed higher concentration of manganese in 87% of DSP positive samples and the expressed per wet weight ranged from 0.15 to 5.38 mg kg⁻¹. The mean concentration of manganese for all DSP positive samples was 1.78 mg kg⁻¹, while for DSP negative samples, it was 48% lower (0.93 mg kg⁻¹). The highest concentration of manganese in DSP positive samples was measured in February 2011. Since the low concentrations of lipophilic biotoxins gymnodimines (GYMs) and spirolides (SPXs) were also detected in the analysed DSP positive samples in the parallel studies, the results obtained in this study suggest future investigations of the connection between the concentration of manganese and lipophilic biotoxins. Full article

An overwhelming amount of evidence now suggests that some people are becoming overloaded with neurotoxins. This is mainly from changes in their living environment and style, coupled with the fact that all people are different and display a broad distribution of genetic susceptibilities. It is important for individuals to know where they lie concerning their ability to either reject or retain toxins. Everyone is contaminated with a certain baseline of toxins that are alien to the body, namely aluminum, arsenic, lead, and mercury. Major societal changes have modified their intake, such as vaccines in enhanced inoculation procedures and the addition of sushi into diets, coupled with the ever-present lead, arsenic, and traces of manganese. It is now apparent that no single toxin is responsible for the current neurological epidemics, but rather a collaborative interaction with possible synergistic components. Selenium, although also a neurotoxin if in an excessive amount, is always present and is generally more present than other toxins. It performs as the body’s natural chelator. However, it is possible that the formation rates of active selenium proteins may become overburdened by other toxins. Every person is different and it now appears imperative that the medical profession establish an individual’s neurotoxicity baseline. Moreover, young women should certainly establish their baselines long before pregnancy in order to identify possible risk factors. Full article

Manganese, as an essential trace element, participates in many physiological reactions by regulating Mn associated enzymes. Magnaporthe oryzae is a serious pathogen and causes destructive losses for rice production. We identified a cytochrome P450 gene, MoMCP1, involving the alleviation of manganese toxin and pathogenicity. To identify the underlying mechanisms, transcriptomics were performed. The results indicated that many pathogenicity related genes were regulated, especially hydrophobin related genes in ∆Momcp1. Furthermore, the Mn²⁺ toxicity decreased the expressions of genes involved in the oxidative phosphorylation and energy production, and increased the reactive oxygen species (ROS) levels, which might impair the functions of mitochondrion and vacuole, compromising the pathogenicity and development in ∆Momcp1. Additionally, our results provided further information about Mn associated the gene network for Mn metabolism in cells. Full article

yonT/SR6 is the second type I toxin-antitoxin (TA) system encoded on prophage SPβ in the B. subtilis chromosome. The yonT ORF specifying a 58 aa toxin is transcribed on a polycistronic mRNA under control of the yonT promoter. The antitoxin SR6 is a 100 nt antisense RNA that overlaps yonT at its 3′ end and the downstream gene yoyJ encoding a second, much weaker, toxin at its 5′ end. SR6 displays a half-life of >60 min, whereas yonT mRNA is less stable with a half-life of ≈8 min. SR6 is in significant excess over yonT mRNA except in minimal medium with glucose. It interacts with the 3′ UTR of yonT mRNA, thereby promoting its degradation by RNase III. By contrast, SR6 does not affect the amount or half-life of yoyJ mRNA. However, in its absence, a yoyJ overexpression plasmid could not be established in Bacillus subtilis suggesting that SR6 inhibits yoyJ translation by directly binding to its ribosome-binding site. While the amounts of both yonT RNA and SR6 were affected by vancomycin, manganese, heat-shock and ethanol stress as well as iron limitation, oxygen stress decreased only the amount of SR6. Full article