Polychlorinated Biphenyls: A Review of Recent Updates on Food Safety and Environmental Monitoring, Health and Toxicological Implications, and Analysis.

A class of organic chemicals known as polychlorinated biphenyls (PCBs) consists of chlorine, hydrogen, and carbon atoms. High boiling points, chemical stability, non-flammability, and insulating properties have enabled them to be used in various industries. Because of their high toxicity, PCBs were one of the first industrial compounds to be banned from production. These compounds have high-fat solubility with bioaccumulation and biomagnification properties in the environment, food chain, and individuals. Hence, they may have an impact not only on individual organisms but ultimately on whole ecosystems. The main sources of PCB exposure are food and environmental pollutants. In the toxicology of PCBs, oxidative stress plays the most influential function. The induction of CYP1A1 due to the high affinity of PCBs for aryl hydrocarbon receptors is considered a trigger for oxidative stress. Production of reactive oxygen species and depletion of glutathione occur due to phase Ⅰ and Ⅱ metabolism, respectively. Thus, cellular redox balance may be disrupted in the presence of PCBs and their metabolites. Chronic and long-term exposure to these compounds can often lead to life-threatening diseases, like diabetes, obesity, cardiovascular and neurological diseases, cancer, and reproductive and endocrine disorders. We present the current knowledge of the routes of PCB exposure and bioaccumulation, the outlook regarding environmental and food safety, the potential role of PCBs in various diseases, the principal mechanisms responsible for PCB toxicity, and the main detection techniques used for PCBs.

The Effect of Levosimendan on Phosphine-Induced Nephrotoxicity: Biochemical and Histopathological Assessment.

BACKGROUND: Aluminum phosphide (AlP) toxicity is associated with a high risk of death due to heart, liver, and kidney failure as the target organs. Phosphine gas released due to the ingestion is the main factor involved in the multi-organ failure with various mechanisms. Levosimendan (LEV) is a calcium sensitizer with a pleiotropic effect on multiple organs. This study aimed to investigate whether LEV can alleviate AlP-induced nephrotoxicity in the rat model. METHOD: Six groups included control group (almond oil only), sole LEV group (48 µg/kg), AlP group (LD50=10 µg/kg), and the poisoned groups treated with LEV at doses of 12, 24, and 48 µg/kg 30 min after AlP gavage. After 24 hours of treatment, serum and kidney samples were taken for biochemical and histopathological analyses. RESULT: Biochemical analysis of the AlP group showed that the activity of complexes I, II, and IV was significantly reduced, while the levels of lipid peroxidation (LPO) and reactive oxygen species (ROS), lactate, and myeloperoxidase (MPO) activity significantly increased. Also, AlP reduced live renal cells and elevated necrosis. However, the levels of serum creatinine and blood urea nitrogen were not affected by the poisoning. LEV co-treatment could increase mitochondrial complex activity and reduce MPO activity, LPO, ROS, and lactate levels. Additionally, the histopathological analysis showed the detrimental effects of AlP on kidney tissue, which was mitigated by LEV administration. CONCLUSION: Our findings showed that LEV can potentially improve oxidative stress, imbalance in the redox status, necrosis, and pathological injuries in kidney tissue following AlP-poisoning.