Environ Int
Department of Occupational and Environmental Health and State Key Laboratory of Environmental Health for Incubating, School of Public Health, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China. Electronic address:
Published: August 2024
Emerging evidence has linked arsenic exposure and metabolic homeostasis, but the mechanism is incompletely understood, especially at relatively low concentrations. In this study, we used a mouse model to evaluate the health impacts and metabolic toxicity of arsenic exposure in drinking water at environmentally relevant levels (0.25 and 1.0 ppm). Our results indicated that arsenic damaged intestinal barrier and induced arsenic accumulation, oxidative stress, and pathological changes in the liver and illum. Interestingly, arsenic increased the hepatic triglyceride (TG) and total cholesterol (TC), while reduced serum TG and TC levels. The liver transcriptome found that arsenic exposure caused transcriptome perturbation and promoted hepatic lipid accumulation by regulating the exogenous fatty acids degradation and apolipoproteins related genes. The serum metabolomics identified 74 and 88 differential metabolites in 0.25 and 1.0 ppm, respectively. The KEGG disease and subcellular location analysis indicated that arsenic induced liver and intestinal diseases, and the mitochondrion might be the target organelle for arsenic-induced toxicity. Co-enrichment of transcriptome and metabolome identified 24 metabolites and 9 genes as metabolic toxicity biomarkers. Moreover, 40 male (20 nonalcoholic fatty liver disease (NAFLD) cases and 20 healthy controls) was further selected to validate our findings. Importantly, the significantly changed L-palmitoylcarnitine, 3-hydroxybutyric acid, 2-hydroxycaproic acid and 6 genes of Hadha, Acadl, Aldh3a2, Cpt1a, Cpt2, and Acox1 were found in the NAFLD cases. The results from integrated multi-omics and chemical-protein network analysis indicated that L-palmitoylcarnitine played a critical role in metabolic toxicity by regulating mitochondrial fatty acids β-oxidation genes (Cpt1a, Cpt2). In conclusion, these findings provided new clues for the metabolic toxicity of arsenic exposure at environmentally relevant levels, which involved in the late-life NAFLD development. Our results also contribute to understanding the human responses and phenotypic changes to this hazardous material exposure in the environment.
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http://dx.doi.org/10.1016/j.envint.2024.108819 | DOI Listing |
Toxicol Res (Camb)
January 2025
Yunnan Provincial Key Laboratory of Public Health and Biosafety and School of Public Health, Kunming Medical University, No. 1168 Chunrongxi Road, Chenggong, Kunming, Yunnan 650500, China.
This study explores the role of Argonaute 2 (AGO2) in the induction of apoptosis by arsenic in 16HBE cells and investigates the association between AGO2 expression and arsenic exposure in a human population. By silencing AGO2 with siRNA, we examined its impact on cell viability and apoptosis using CCK-8, HO-PI, and JC-1 assays, complemented by qRT-PCR and Western blot analyses for gene and protein expressions. Our findings revealed a significant correlation between AGO2 expression and levels of exposure to inorganic arsenic (iAs), which was more pronounced than with other arsenic forms such as monomethylarsonic (MMA) and dimethylarsinic acids (DMA).
View Article and Find Full Text PDFClin Kidney J
January 2025
Department of Nephrology, Dialysis, Transplantation, Dr C. I. Parhon Hospital, Iasi, Romania.
The timeless tale of Snow White, with its emphasis on fair skin as a beauty ideal, mirrors a contemporary issue in nephrology: the harmful impact of skin-whitening creams on kidney health. Fairness creams have deeply embedded themselves in global society, driven by a pervasive obsession with lighter skin tones as a symbol of beauty. This widespread use reflects deeply rooted cultural beliefs and social norms, despite the significant health risks associated with these products.
View Article and Find Full Text PDFJ Environ Radioact
January 2025
Belgian Nuclear Research Centre (SCK CEN), Boeretang 200, 2400 Mol, Belgium. Electronic address:
A population model is presented to study the combined effects of ionising radiation and chemical pollutants on wildlife. The model is based on first order, non-linear and logistic differential equations combining mortality, morbidity and reproduction phenomena with life history data and ecological interactions. Acclimation is considered as a possible mechanism to study theoretically this effect at low levels of radiation or chemical concentration.
View Article and Find Full Text PDFJ Nephrol
January 2025
Laboratory of Renal Toxicopathology & Medicine, P.G. Department of Environmental Sciences, Sambalpur University, Burla, Odisha, 768019, India.
Background: The present community-based study assessed the prevalence of chronic kidney disease (CKD)/chronic kidney disease of unknown origin (CKDu) as well as anemia in some intense agricultural zones under Hirakud Command Area and evaluated their association with pesticides and heavy metal exposure.
Methods: Random cluster sampling method was used to assess the prevalence of CKD and anemia. Hematological analysis was carried out using autoanalyzer.
Ecotoxicol Environ Saf
January 2025
East China Sea Fisheries Research Institute, Chinese Academy of Fishery Sciences, Shanghai 200090, China. Electronic address:
Arsenic is a pervasive environmental pollutant that can bioaccumulate in Antarctic krill through the food chain, posing potential risks to human health. This study investigates the toxic effects of arsenic in Antarctic krill oil (AKO) on Caco-2 cells, focusing on oxidative stress and apoptosis induction. AKO is nutrient-rich and contains various arsenic species, including arsenite (As³⁺), arsenate (As⁵⁺), dimethyl arsinic acid (DMA), and arsenobetaine (AsB), each exhibiting different toxic potencies.
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