Search Results (50)

Cadmium (CAD) is a prevalent environmental contaminant that poses serious cardiotoxic risks. The heart, kidney, liver, and brain are just a few of the essential organs that can sustain serious harm from CAD, a very poisonous heavy metal. The cardiotoxic mechanism of CAD is linked to oxidative damage and inflammation. A trace element with anti-inflammatory, anti-apoptotic, and antioxidant qualities, selenium (SEL) can be taken as a dietary supplement. The biotoxicity of heavy metal CAD is significantly inhibited by SEL, a mineral that is vital to human and animal nutrition. Through ROS-induced PARP-1/ADPR/TRPM2 pathways, this study seeks to assess the preventive benefits of selenium against cardiovascular damage caused by CAD. The SEL showed encouraging results in reducing inflammatory and oxidative reactions. Rats were given 0.5 mg/kg SEL and 3 mg/kg 2-Aminoethyl diphenylborinate (2-APB) intraperitoneally for five days, in addition to 25 mg/kg CAD given via gavage. Histopathological examination findings revealed that the morphologic changes in the hearts of the CAD group rats were characterised by marked necrosis and the degeneration of myocytes and congestion of vessels. Compared to the rats in the CAD group, the hearts of the SEL, 2-APB and SEL+2-APB groups showed fewer morphological alterations. Moreover, in rats given CAD, there was an increase in cardiac malondialdehyde (MDA), total oxidant (TOS), reactive oxygen species (ROS), caspase (Casp-3-9), and TNF-α, whereas glutathione (GSH), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and total antioxidant (TAS) decreased. SEL improved antioxidants, avoided tissue damage, and reduced cardiac MDA, TOS, and ROS. In rats given CAD, SEL decreased cardiac PARP-1, TRPM2, TNF-α, and caspase. In summary, by reducing oxidative stress and cardiac damage and modifying the ROS/PARP-1/TRPM2 pathway, SEL protected against CAD cardiotoxicity. Full article

The heavy metal cadmium (Cd) affects the global livestock production economy mainly through the contamination of feed raw materials and secondary contamination in feed processing, and it also poses a serious threat to food safety and human health. The nucleotide-binding oligomerization domain-like pyrin-domain-containing protein 3 (NLRP3) inflammasome is a key regulatory element of pyroptosis, which is engaged in kidney injury. Meanwhile, autophagy is also involved in renal inflammation. Mammalian target of rapamycin (mTOR) plays an important role in pyroptosis and autophagy, but its function in Cd-induced kidney injury remains unclear. In this study, we explored the role of mTOR-mediated autophagy and pyroptosis in kidney injury caused by Cd exposure and elucidated its underlying mechanism. Our data showed that Cd exposure reduced the integrity of kidney cell membranes, increased the expression of pyroptosis-associated proteins, and promoted the release of inflammatory cytokines. Subsequently, a notable attenuation in Cd-induced pyroptosis was observed following the administration of CY-09, an NLRP3 inhibitor. In addition, Cd exposure promoted autophagy in kidney cells. Importantly, in both in vivo and in vitro experiments, rapamycin, an mTOR inhibitor, downregulated the expression of pyroptosis-related proteins, thereby significantly improving Cd-induced kidney injury. In summary, our results indicate that mTOR-mediated autophagy has a significant protective effect on NLRP3 inflammasome-dependent kidney injury induced by Cd exposure, thus providing new insights into the prevention and treatment of Cd poisoning. Full article

Water pollution is a significant problem stemming from several causes, with the contamination of heavy metal(oid)s being a primary concern. This is especially concerning because of the poisonous characteristics of these metal(oid)s and their effects on the aquatic ecosystem. This research is distinguished by its unique methodology for assessing metal(oid)s in the surface water of Bangladeshi rivers over a period of sixteen years, from 2007 to 2022. This work seeks to elucidate recent results on metal(oid) concentrations, contamination levels, multivariate statistical analyses, source identification using positive matrix factorization models, and probabilistic health risks. The findings reveal that the concentrations of chromium, nickel, arsenic, cadmium, and lead exceeded the acceptable limits for drinking water established by the World Health Organization (WHO) by factors of 4.64, 2.25, 22.51, 45.60, and 10.13, respectively. Our meta-analysis, subsequent to a Principal Component Analysis, indicated that increased concentrations of hazardous metals account for 85.47% of the variation from both anthropogenic and natural causes. Ecological risk indicators, including the metal index (84.06) and the Nemerow pollution index (10.55), indicated significant metal contamination. Ecological risk indicators, like the metal index (84.06) and the Nemerow pollution index (10.55), indicate substantial metal contamination. The positive matrix factorization (PMF) model detected the following sources of metals in water: industrial (22%), mixed (32%), agricultural activities (27%), and natural sources (19%). Furthermore, Monte Carlo-simulation-based assessments of health hazards indicated that the mean hazard index (HI) and cancer risk values for adults (301.89 and 422.76) and children (51.56 and 39.45) significantly exceeded the recommended limits, suggesting that both adults and children are vulnerable to potential non-carcinogenic and carcinogenic health risks. The immediate execution of control measures and regulations is essential to avert escalating pollution in surface water, protect ecosystems, and mitigate health hazards. Full article

Cadmium (Cd) is a pervasive environmental and industrial toxin that poses significant health risks. It readily moves through soil–plant systems, leading to global contamination and human exposure through diet, smoking, and pollution. The main purpose of this review is to explore the effect of Cd on physiological processes of different bodies’ organs, including the bones, kidneys, and liver, as well as the immune, cerebrovascular, cardiovascular, and reproductive systems. Accumulation of Cd in the body can result in poisoning with severe impacts on bone and kidney health, as well as reduced bone mineral density due to renal damage. Research has linked Cd to lung cancer and pulmonary toxicity, and elevated urinary biomarkers suggest compromised renal function. Cd also affects the cardiovascular, cerebrovascular, and immune systems; the liver; and reproductive systems, contributing to various diseases by disrupting blood pressure and calcium regulation, causing oxidative stress and DNA damage, and impairing cell functions. Ongoing research is essential to fully understand Cd-induced toxicological effects and to develop effective interventions to prevent exposure and mitigate health risks. Full article

Hazardous heavy metals, particularly cadmium (Cd), are widely distributed in the environment and cause oxidative stress in various animal and human organs. Clove oil (CLO), a common aromatic spice, has been used as a traditional medication as it has potent anti-inflammatory, antioxidant, and hepatoprotective properties. Background/Objectives: This study aimed to investigate the antioxidant, antiapoptotic, and anti-inflammatory effects of clove oil (CLO) against hepatorenal toxicity induced by cadmium (Cd). Methods: Twenty rats were equally divided into four groups: a control group, a Cd group treated with 15 mg/kg b.wt CdCl₂, a CLO group administered 200 mg/kg b.wt CLO, and a Cd+CLO group. All groups were orally treated for 4 weeks. Results: Cadmium (Cd) exposure caused anemia and hepatorenal damage, as evidenced by increased serum levels of urea, creatinine, uric acid, total bilirubin (including its direct and indirect fractions), and elevated activities of liver enzymes such as alanine transaminase (ALT), aspartate transaminase (AST), and alkaline phosphatase (ALP). However, total protein and albumin levels decreased. Furthermore, there was a decrease in the levels of glutathione, glutathione transferase, and catalase in the liver antioxidant profiles. Meanwhile, malondialdehyde levels increased. Cadmium toxicity caused elevated expression of liver apoptosis markers, such as tumor necrosis factor-alpha (TNF-α) and caspase-3, and inflammation. CLO ameliorated the oxidative effects of Cd through decreasing urea (27.4%), creatinine (41.6%), liver enzymes, and hepatic apoptotic markers while increasing levels of total protein, albumin, and hepatic values of SOD (60.37%), CAT (64.49%), GSH (50.41%), and GST (9.16%). Conclusions: Hematological and biochemical parameters, as well as the antioxidant system, improved following clove oil treatment, leading to a reduction in hepatorenal damage. Therefore, it is possible to conclude that CLO protects rats from inflammation, apoptosis, and hepatorenal oxidative damage caused by Cd poisoning. Comprehensive translational research is required to validate CLO’s efficacy and safety of use in humans. Future studies should focus on elucidating the precise molecular mechanisms, optimal dosing strategies, and potential synergistic effects of CLO with other therapeutic agents. Full article

This study was aimed at extracting, characterizing, and exploring the detoxification activity of the peptide-containing polysaccharide from Agaricus balchaschensis. An anion adsorption fraction was acquired through hot water extraction. Its structure was analyzed, and the potential protective effect against cadmium-intoxicated mice was explored. Structural analysis revealed that the principal component of the peptide-containing polysaccharide of A. balchaschensis (ABPCP) is polysaccharide, which consists of glucose, mannose, galactose, and xylose, containing (1 → 4)-linked α-D-glucan, (1 → 3)-linked β-D-Glcp, (1 → 4)-linked β-D-Glcp, (1 → 6)-linked β-D-Glcp, (1 → 6)-linked β-D-Manp, (1 → 3)-linked β-D-Galp, (1 → 6)-linked β-D-Galp, and (1 → 4)-linked β-D-xylan. The amino acid content of ABPCP is 11.747 mg/g. Threonine, serine, glutamate, glycine, alanine, cysteine, valine, methionine, lysine, and arginine were detected in ABPCP, among which the content of glutamate was the highest. The alleviating effect of ABPCP on cadmium poisoning in mice was investigated. ABPCP significantly reduced the cadmium content in serum and the heart, kidneys, and liver, which indicates that ABPCP could promote cadmium discharge. ABPCP also significantly decreased serum nitric oxide, endothelin-1, urea, uric acid, and serum creatinine, alleviating kidney and liver damage caused by cadmium. All these results manifest that ABPCP can lower the cadmium content in organs and alleviate the damage to kidneys and livers damaged by Cd. Full article

Microplastics pollution in freshwater systems is attracting increasing attention. However, our knowledge of its combined toxicity with heavy metals is scarce. In this study, Rana zhenhaiensis was used as the model animal to study the combined poisoning mechanism of cadmium or microplastics on the digestive systems of tadpoles in freshwater. Results showed that the exposure to cadmium and polystyrene increased the mortality and metamorphosis rate of R. zhenhaiensis tadpoles, and delayed their growth and development. Cadmium was detected in the livers and intestines, while polystyrene mainly accumulated in the gills and intestines of tadpoles. The individual exposure of cadmium or polystyrene can cause pathological damage to liver tissue, induce oxidative stress in liver, and change gene expression. Cadmium co-exposure with polystyrene can reduce the cadmium accumulation in the liver. While polystyrene can slightly increase cadmium accumulation in the intestine. Exposure to cadmium and polystyrene altered the abundance and community structure of intestinal microbiota, and polystyrene increased the dysregulation of the gut microbiome. In this study, the combined exposure of microplastics and cadmium had a negative impact on R. zhenhaiensis tadpoles, but the introduction of microplastics on the toxicity of cadmium on the tadpoles needs further investigation, due to the different characteristics of microplastics. Full article

The transition metal cadmium (Cd) is toxic to humans and can induce cellular redox stress and inflammation. Cd is a recognized carcinogen, but the molecular mechanisms associated with its genotoxicity and carcinogenicity are not defined. Therefore, a systematic review was undertaken to examine the scientific literature that has covered the molecular mechanism of Cd genotoxicity and its relationship to cellular redox stress and inflammation. An electronic database search of PubMed, Scopus, and the Web of Science Core Collection was conducted to retrieve the studies that had investigated if Cd genotoxicity was directly linked to the induction of redox stress and inflammation. Studies included exposure to Cd via in vitro and in vivo routes of administration. Of 214 publications retrieved, 10 met the inclusion criteria for this review. Preclinical studies indicate that Cd exposure causes the induction of reactive oxygen species (ROS) and, via concomitant activity of the transcription factor NF-κβ, induces the production of pro-inflammatory cytokines and a cytokine profile consistent with the induction of an allergic response. There is limited information regarding the impact of Cd on cellular signal transduction pathways, and the relationship of this to genotoxicity is still inconclusive. Nevertheless, pre-incubation with the antioxidants, N-acetylcysteine or sulforaphane, or the necroptosis inhibitor, necrostatin-1, reduces Cd toxicity; indicative that these agents may be a beneficial treatment adjunct in cases of Cd poisoning. Collectively, this review highlights that Cd-induced toxicity and associated tissue pathology, and ultimately the carcinogenic potential of Cd, may be driven by redox stress and inflammatory mechanisms. Full article

Ganoderma triterpenes and spore powder have shown promising results in mitigating cadmium-induced renal and hepatic injuries. Ganoderma lucidum active peptide GLP4 is a natural protein with dual antioxidant activities derived from the mycelium of Ganoderma lucidum. However, its efficacy in alleviating cadmium-induced lung injury remains unexplored. This study aims to investigate the protective effects of GLP4 against cadmium-induced lung injury in mice. Mice were exposed to cadmium chloride via nebulization to induce lung injury. The protective effect of GLP4 was assessed by measuring the total cell count in BALF, levels of inflammatory cytokines, and the expression of NLRP3 in lung tissues a through histopathological examination of lung tissue changes. The results showed that GLP4 significantly mitigated histopathological damage in lung tissues, decreased the secretion of inflammatory cytokines, and reduced the expression of NLRP3, which was elevated in cadmium-exposed mice. In vitro studies further revealed that GLP4 inhibited the cadmium-induced activation of the NLRP3 inflammasome. Notably, acute cadmium exposure by the respiratory tract did not affect the liver and kidneys of the mice. The findings suggest that GLP4 reduces cadmium-induced lung injury in mice by inhibiting the activation of the NLRP3 inflammasome, which provides a theoretical foundation for using Ganoderma lucidum as a preventive and therapeutic agent against cadmium poisoning. Full article

Cadmium (Cd) is recognized as being linked to several liver diseases. Currently, due to the limited spectrum of drugs available for the treatment of Cd intoxication, developing and designing antidotes with superior detoxification capacity and revealing their underlying mechanisms remains a major challenge. Therefore, we developed the first next-generation probiotic E. coli 1917-pSK18a-MT that delivers metallothionein (MT) to overcome Cd-induced liver injury in C57BL/6 mice by utilizing bacterial surface display technology. The results demonstrate that E. coli 1917-pSK18a-MT could efficiently express MT without altering the growth and probiotic properties of the strain. Moreover, we found that E. coli 1917-pSK18a-MT ameliorated Cd contamination-induced hepatic steatosis, inflammatory cell infiltration, and liver fibrosis by decreasing the expression of aminotransferases along with inflammatory factors. Activation of the Nrf2-Keap1 signaling pathway also further illustrated the hepatoprotective effects of the engineered bacteria. Finally, we showed that E. coli 1917-pSK18a-MT improved the colonic barrier function impaired by Cd induction and ameliorated intestinal flora dysbiosis in Cd-poisoned mice by increasing the relative abundance of the Verrucomicrobiota. These data revealed that the combination of E. coli 1917 and MT both alleviated Cd-induced liver injury to a greater extent and restored the integrity of colonic epithelial tissues and bacterial dysbiosis. Full article

Heavy metal poisoning has a life-threatening impact on the human body to aquatic ecosystems. This necessitates designing a convenient green methodology for the fabrication of an electrochemical sensor that can detect heavy metal ions efficiently. In this study, boron (B) and nitrogen (N) co-doped laser-induced porous graphene (LIG_BN) nanostructured electrodes were fabricated using a direct laser writing technique. The fabricated electrodes were utilised for the individual and simultaneous electrochemical detection of lead (Pb²⁺) and cadmium (Cd²⁺) ions using a square wave voltammetry technique (SWV). The synergistic effect of B and N co-doping results in an improved sensing performance of the electrode with better sensitivity of 0.725 µA/µM for Pb²⁺ and 0.661 µA/µM for Cd²⁺ ions, respectively. Moreover, the sensing electrode shows a low limit of detection of 0.21 µM and 0.25 µM for Pb²⁺ and Cd²⁺ ions, with wide linear ranges from 8.0 to 80 µM for Pb²⁺ and Cd²⁺ ions and high linearity of R² = 0.99 in case of simultaneous detection. This rapid and facile method of fabricating heteroatom-doped porous graphene opens a new avenue in electrochemical sensing studies to detect various hazardous metal ions. Full article

Polysaccharides are functional foods or drugs that can be used to alleviate heavy metal poisoning by cadmium, lead, mercury, and arsenic. Industries generate substantial quantities of toxic heavy metal wastes, such as wastewater discharges, paints, electronic waste, batteries, pigments, and plastics, into the environment that pose a risk to human health. Therefore, it is imperative to eliminate accumulated heavy metal ions from the body and the environment. Heavy metal toxicity can lead to decreased energy levels and impair the functioning of vital organs, such as the brain, lungs, kidneys, liver, and blood. Prolonged exposure can result in progressive physical, muscular, and neurological degeneration that resembles conditions such as multiple sclerosis, Parkinson’s disease, Alzheimer’s disease, and muscular dystrophy. Polysaccharides operate through mechanisms such as chelation, antioxidant defense, immunomodulation, and tissue repair. Polysaccharides involved in heavy metal removal include methionine and cysteine, together with N-acetylcysteine, an acetylated form of cysteine, S-adenosylmethionine, a metabolite of methionine, α-lipoic acid, and the tripeptide glutathione (GSH). These compounds effectively bind with harmful heavy metals to create a stable complex and defend biological targets from metal ions, thus decreasing their harmful effects and causing them to be excreted from the body. This review also highlights the importance of polysaccharides’ ability to mitigate oxidative stress, enhance immune responses, and support tissue repair processes. Polysaccharides are ubiquitous in nature and take part in diverse processes, making them potential natural therapies for heavy metal-related diseases. This review discusses the effectiveness of natural polysaccharides and the mechanisms that allow them to bind with heavy metals to alleviate their effects from the body and the environment. Polysaccharides have inherent features that enable them to function as pharmacological agents and regulate the immune response. Full article

Cadmium (Cd) is an environmental pollutant, widely existing in soil, and can be absorbed and accumulated by plants. Hunan Province exhibits the worst cadmium contamination of farmland in China. Ruminants possess an abundant microbial population in the rumen, which enables them to tolerate various poisonous plants. To investigate whether the rumen microbiota could respond to Cd and mitigate the toxicity of Cd-accumulated maize to ruminants, 6-month-old cattle were fed with 85.82% (fresh basis) normal whole-plant maize silage diet (CON, n = 10) or Cd-accumulated whole-plant maize silage diet (CAM, n = 10) for 107 days. When compared to the CON cattle, CAM cattle showed significantly higher gain-to-feed ratio and an increased total bacterial population in the rumen, but a decreased total bacterial population in the colon. CAM cattle had higher relative abundance of Prevotella and Lachnospiraceae ND3007 group in the rumen, and Lachnospiraceae NK4A136 group and Clostridia vadinBB60 group in the colon. Notably, microbial correlations were enhanced in all segments of CAM cattle, especially Peptostreptococcaceae in the jejunum. Transcriptome analysis revealed down-regulation of several immune-related genes in the rumen of CAM cattle, and differentially expressed genes in the rumen were mostly involved in immune regulation. These findings indicated that feeding Cd-accumulated maize diet with a Cd concentration of 6.74 mg/kg dry matter (DM) could stimulate SCFA-related bacteria in the rumen, induce hormesis to promote weight gain, and improve energy utilization of cattle. Full article

Cadmium (Cd) is a ductile metal in the form of a blueish or silvery-white powder. It is naturally found in soil (about 0.2 mg/kg), minerals, and water. Cd belongs to the group of toxic, carcinogenic, and stimulating elements. Its biological half-life in the human body ranges from 16 to even 30 years on average. Some lung diseases (such as emphysema, asthma, and bronchitis) and high blood pressure are thought to be related to slow poisoning. The symptoms of cadmium poisoning may vary depending on the time of exposure, the type of diet, and the age and health status of the exposed people. For non-smokers and non-occupational exposures, the only source of exposure is diet. The FAO/WHO recommends that the tolerable cadmium intake for an adult is approximately 0.4–0.5 mg/week (60–70 µg per day). Cadmium is primarily absorbed through the respiratory system (about 13–19% of Cd from the air), but it can also enter through the digestive system (about 10–44%), when dust is mixed and swallowed with saliva. The amount of accumulated Cd ranges from 0.14 to 3.2 ppm in muscles, 1.8 ppm in bones, and 0.0052 ppm in the blood. People who are most frequently exposed to heavy metals should be continuously monitored in order to maintain a healthy lifestyle, as well as to implement effective preventive measures and improve public health. Full article

Food safety and environmental pollution are the hotspots of general concern globally. Notably, long-term accumulation of trace toxic heavy metals, such as cadmium (Cd), in animals may endanger human health via the food chain. The mechanism of Cd toxicity in the goat, a popular farmed animal, has not been extensively investigated to date. Therefore, in this study, ten male goats (Nubian black goat × native black goat) were exposed to Cd via drinking water containing CdCl₂ (20 mg Cd·kg⁻¹·BW) for 30 days (five male goats per group). In this study, we used an integrated approach combining proteomics and metabolomics to profile proteins and metabolites in the serum of Cd-exposed goats. It was found that Cd exposure impacted the levels of 30 serum metabolites and 108 proteins. The combined proteomic and metabolomic analysis revealed that Cd exposure affected arginine and proline metabolism, beta-alanine metabolism, and glutathione metabolism. Further, antioxidant capacity in the serum of goats exposed to Cd was reduced. We identified CKM and spermidine as potential protein and metabolic markers, respectively, of early Cd toxicity in the goat. This study details approaches for the early diagnosis and prevention of Cd-poisoned goats. Full article