11/19/2022 0 Comments School mate 2 controls![]() ![]() Hepatocellular carcinoma (HCC) accounts for approximately 75% of all liver cancers, and hepatitis virus remains the most important global risk factor for HCC. Globally, liver cancer ranks third in terms of mortality, and among males, it is the second leading cause of cancer death. In 2020, more than 905,677 new liver cancer cases were registered worldwide, accounting for 4.7% of overall cancer incidence. The effects of long-term Cd exposure include increased risks of cardiovascular disorders, obesity, diabetes, and cancer. Cd damages various organs, with major effects on the kidneys and the liver. Ingestion is the main source of Cd in individuals without occupational and smoking exposure. ![]() IntroductionĬadmium (Cd) is a nonessential trace metal recognized as one of the top 20 hazardous substances to humans through occupational and environmental exposure. These findings suggest that early-life exposure to low-dose cadmium accelerates liver cancer development induced by a DEN/HFCD in male mice, probably due to chronic lipotoxicity and inflammation caused by increased uptake but decreased consumption of fatty acids. The liver peritumor tissue of early-life cadmium-exposed mice exhibited greater inflammation and disruption of fatty acid metabolism, accompanied by higher malondialdehyde and lower esterified triglyceride levels compared to mice without cadmium exposure. ![]() In contrast, in male mice, early-life cadmium exposure enhanced liver cancer induction by DEN/HFCD with high incidence and larger liver tumors. For females, early-life cadmium exposure also worsened insulin intolerance but did not significantly promote DEN/HFCD diet-induced liver tumors. Both male and female cadmium-exposed mice showed increased body weight compared to non-cadmium-treated mice. However, by 26 and 29 weeks of age, hepatic cadmium fell to control levels, while a significant decrease was observed in copper and iron in the liver. Before weaning, liver cadmium levels were significantly higher in mice with early-life cadmium exposure than in those without cadmium exposure. HCC in C57BL/6J mice was induced by diethylnitrosamine (DEN) injection at weaning, followed by a long-term high-fat choline-deficient (HFCD) diet. This study investigated the impact of early-life exposure to cadmium on the incidence and potential mechanisms of hepatocellular carcinoma (HCC) in offspring subjected to postweaning HCC induction. However, whether maternal cadmium exposure accelerates liver cancer in the offspring is unknown. Maternal exposure to cadmium causes obesity and metabolic changes in the offspring, including nonalcoholic fatty liver disease-like pathology. ![]()
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