Toxic effects of Aroclor 1254 on rat liver and modifying roles of selenium

Polychlorinated biphenyls (PCBs) were used in different industrial areas and banned due to their high toxicity. Aroclor 1254 (A1254), commercial PCB congener, accumulates in environment leading to high human exposure. A1254 may cause hepatotoxicity, metabolic and endocrine disorders. In our study, 3-week-old male rats were separated into 6 groups: C (0.15 mg/kg Se in diet); SeS (1 mg/kg Se in diet); SeD (0.05 mg/kg Se in diet); A1254 receiving groups (A; ASeS; ASeD) were given 10 mg/kg/day A1254 orally for last 15 days of feeding period with control, SeD or SeS diet, respectively, for 5 weeks. Histopathology, oxidant/antioxidant balance, apoptosis and cell cycle proteins (p53, p21) in liver were evaluated. Our results suggest that A1254 leads to changes in histology, oxidative stress and apoptosis. Selenium deficiency augments oxidative stress and apoptosis while selenium supplementation is partially protective. More mechanistic in vivo experiments are necessary for evaluation of hepatotoxicity of PCBs.

Automated summary

Polychlorinated biphenyls (PCBs) were widely used in various industries but were later banned due to their high toxicity. Aroclor 1254 (A1254), a commercial PCB congener, accumulates in the environment, leading to high human exposure. A1254 has been found to cause hepatotoxicity, metabolic disorders, and endocrine disorders. Our study on male rats showed that A1254 resulted in histological changes, oxidative stress, and apoptosis in the liver. Selenium deficiency aggravated oxidative stress and apoptosis, while selenium supplementation provided partial protection. More mechanistic in vivo experiments are needed to further evaluate the hepatotoxicity of PCBs.