Copper toxicity in the liver of broiler chicken: insights from metabolomics and AMPK-mTOR mediated autophagy perspective

Poultry Science, Journal Year: 2024, Volume and Issue: 103(9), P. 104011 - 104011

Published: June 22, 2024

Exposure to copper (Cu) has been associated with metabolic disorders in animals and humans, but the underlying mechanism remains unclear. One-day-old broiler chickens, numbering a total of 192, were nourished dietary intakes that contained varying concentrations Cu, specifically 11, 110, 220, 330 mg/kg for period extending over duration 7 wk. As result study, Cu exposure resulted vacuolization, fragmentation mitochondria cristae, increase autophagosomes hepatocytes. Metabolomics analysis illustrated caused 59 different metabolites liver, predominantly glycerophospholipid pathway, leading disruption. Moreover, high-Cu diet markedly reduced levels AMPKα1, p-AMPKα1, mTOR, p-mTOR enhanced expression autophagy-related factors (Atg5, Dynein, Beclin1, LC3-II). Overall, chicken liver injury disturbed processes mediated autophagy primarily through AMPK-mTOR axis.

Language: Английский

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Assessing the hepatotoxicity of phosphogypsum leachate in zebrafish (Danio rerio)

The Science of The Total Environment, Journal Year: 2024, Volume and Issue: 926, P. 172018 - 172018

Published: March 27, 2024

Language: Английский

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Environment, Endocrine Disruptors, and Fatty Liver Disease Associated with Metabolic Dysfunction (MASLD)

Metabolites, Journal Year: 2024, Volume and Issue: 14(1), P. 71 - 71

Published: Jan. 22, 2024

Ecological theories suggest that environmental factors significantly influence obesity risk and related syndemic morbidities, including metabolically abnormal associated with nonalcoholic fatty liver disease (MASLD). These encompass anthropogenic influences endocrine-disrupting chemicals (EDCs), synergistically interacting to induce metabolic discrepancies, notably in early life, disrupt processes adulthood. This review focuses on endocrine disruptors affecting a child’s MASLD risk, independent of their role as obesogens thus regardless impact adipogenesis. The plays pivotal detoxification processes, where various lipophilic molecules accumulate parenchyma, exacerbating inflammation functioning new anthropogenics perpetuate chronic low-grade inflammation, especially insulin resistance, crucial the pathogenesis MASLD.

Language: Английский

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Kidney function mediates the association of per- and poly-fluoroalkyl substances (PFAS) and heavy metals with hepatic fibrosis risk

Environmental Research, Journal Year: 2024, Volume and Issue: unknown, P. 120092 - 120092

Published: Sept. 1, 2024

Language: Английский

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The association between endocrine disrupting chemicals and nonalcoholic fatty liver disease: A systematic review and meta-analysis

Pharmacological Research, Journal Year: 2024, Volume and Issue: 205, P. 107251 - 107251

Published: June 12, 2024

Nonalcoholic fatty liver disease (NAFLD) is one of the leading causes chronic worldwide. Epidemiological studies have reported that exposure population to environmental endocrine-disrupting chemicals (EDCs) associated with NAFLD. However, EDCs are different types, and there inconsistencies in relevant evidence descriptions, which not been systematically summarized so far. Therefore, this study aimed determine association between Three databases, including PubMed, Web science, Embase were searched, 27 articles included study. Methodological quality, heterogeneity, publication bias assessed using Newcastle-Ottawa scale, I

Language: Английский

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The association of urinary heavy metal exposure with frailty susceptibility and mortality in middle-aged and older adults: a population-based study

Archives of Public Health, Journal Year: 2024, Volume and Issue: 82(1)

Published: March 27, 2024

Abstract Heavy metals’ presence as environmental pollutants has a close link to adverse health effects. Frailty, clinical syndrome hallmarked by elevated vulnerability stressors, presents substantial challenge in healthcare. However, the association between exposure heavy metals and frailty largely remains unexplored. Utilizing data from National Health Nutrition Examination Survey (NHANES) spanning 2003–2018 correlated with U.S. Death Index (NDI) 2019, we investigated mortality outcomes. Logistic regression, Cox Kaplan-Meier survival curves, weighted quantile-sum (WQS) Bayesian kernel machine regression (BKMR) were employed assess metal incidence frail population. Eight measured urine using inductively coupled plasma mass spectrometry values adjusted for urinary creatinine, which was used reflect exposure. The cohort incorporated 5370 female participants aged 45 above, 1518 diagnosed frailty. findings indicated correlation specific metals, namely tungsten (odds ratio [OR]: 1.94, 95% confidence interval [CI]: 1.31–2.89), cobalt (OR: 1.64, CI: 1.40–1.93), cadmium 1.93, 1.52–2.43), uranium 7.36, 1.53–35.28), an risk of WQS BKMR models identified cadmium, cobalt, main contributors analysis, after adjustment covariates, suggested that higher levels lead, death patients, associated hazard ratios (HR) 1.96 (1.53, 2.52) 1.30 (1.13, 1.49), respectively. Our study revealed significant positive mixtures onset middle-aged older adults, along increased patients. Cobalt, emerged prominent frailty, directly impacting long-term life expectancy

Language: Английский

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Impact of arsenic exposure on the hepatic metabolic molecular network in obese pregnant mice using metabolomics and proteomics

Chinese Journal of Chromatography, Journal Year: 2025, Volume and Issue: 43(1), P. 50 - 59

Published: Jan. 1, 2025

Arsenic is a ubiquitous environmental toxin that can affect normal physiological processes. Although the health impacts of arsenic have been investigated, its influence on hepatic metabolism in obese pregnant women and underlying mechanisms remain unclear. Multi-omics analysis, including metabolomics proteomics, improve understanding arsenic-induced hepatotoxicity women. This study aimed to investigate adverse effects gestational exposure high-fat-diet-induced mice. Following during pregnancy, liver tissue was evaluated comprehensively using proteomics techniques combined with pathological biochemical analyses. not only significantly increased lipid accumulation livers mice but also elevated inflammatory factors oxidative stress markers. Specifically, histopathological examination revealed more steatosis, cell infiltration, hepatocyte ballooning arsenic-exposed than those controls. These changes indicate exacerbates induces damage context obesity. Metabolomic analysis provided further insight into metabolic-level disruption caused by exposure. Significant were observed pathways, particularly arachidonic acid pathway. As metabolites play important roles inflammation stress, this pathway may be critical hepatotoxicity. Additionally, proteomic showed differences expression levels several key proteins involved synthesis, response. Notably, oxidative-stress-related proteins, glutathione peroxidase 4 (GPX4), upregulated, suggesting an burden. In summary, there are complex interaction among exposure, response, related metabolism. The integration aided clarifying molecular alterations induced arsenic. results show affects through multiple metabolic pathways protein regulatory mechanisms. addition providing new insights relationship between obesity as well diseases, act reference for risk assessment formulation public policies. enhanced will contribute development strategies mitigating risks associated toxins, vulnerable groups such

Language: Английский

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Arsenic Exposure Triggers Nonalcoholic Fatty Liver Disease through Repressing S-Adenosylmethionine-Dependent Histone Methylation in Rats

Environmental Science & Technology, Journal Year: 2025, Volume and Issue: 59(1), P. 268 - 278

Published: Jan. 2, 2025

Arsenic (As) is a toxic metalloid widespread in the environment, and its exposure has been associated with variety of adverse health outcomes. As demonstrated to cause nonalcoholic fatty liver disease (NAFLD), underlying epigenetic mechanisms remain largely unknown. This study aimed investigate roles histone modifications low-level exposure-induced NAFLD rats. The results showed that caused lipid accumulation upregulated expression metabolism-related genes Fabp1, Srebf1, Apoc3, while downregulated Acox1 Cpt1a rat liver. In addition, it was found inorganic arsenite (iAsIII) methylated DMA, S-adenosylmethionine (SAM) level decreased, which would contribute repression H3K9me1/2 after exposure. vitro studies revealed SAM supplementation attenuated by restoring HepG2 cells, further confirmed our animal results. Therefore, suggested methylation depleted SAM, inhibited activated Apoc3 expressions, leading upon Overall, these data shed new light on role SAM-mediated As-triggered NAFLD, could be useful for prevention intervention hepatotoxicity induced environmental

Language: Английский

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Dietary protein intake and PM2.5 on ovarian cancer survival: A prospective cohort study

Ecotoxicology and Environmental Safety, Journal Year: 2025, Volume and Issue: unknown, P. 117798 - 117798

Published: Jan. 1, 2025

Language: Английский

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α‐Lipoic Acid Ameliorates Arsenic‐Induced Lipid Disorders by Promoting Peroxisomal β‐Oxidation and Reducing Lipophagy in Chicken Hepatocyte

Advanced Science, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 30, 2025

Abstract Liver disease poses a significant threat to global public health, with arsenic (As) recognized as major environmental toxin contributing liver injury. However, the specific mechanisms and protective effects of α‐lipoic acid (LA) remain unclear. Therefore, this study employs network toxicology pharmacology comprehensively analyze hepatotoxic mechanism As hepatoprotective LA, further verifies peroxisomal β‐oxidation lipophagy in process. The analysis results show that induces damage mainly through autophagy, apoptosis, lipid metabolism, oxidative stress, whereas LA exerts its properties by regulating metabolism. Further verifications find inhibits SIRT1 expression, activates P53 Notch pathways, damages mitochondria, β‐oxidation, increases accumulation, enhances liver, while intervention alleviates As‐induced accumulation targeting SIRT1, ameliorating mitochondrial damage, enhancing thereby alleviating damage. This clarifies hepatotoxicity provides theoretical basis for potential agent.

Language: Английский

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