Effects of sub-acute aluminium phosphide exposure on hepatorenal biomarkers and antioxidant defense in rats
TL;DR
Investigating the dose-dependent toxicity of AlP on biochemical biomarkers, antioxidant defense responses, and histological changes in rat liver and kidneys found sub-acute AlP exposure caused dose-dependent liver and kidney toxicity, high doses induced pronounced damage, and low doses showed mild or minimal effects.
Abstract
Aluminium phosphide (AlP) is a well-known toxic pesticide, but its dose-dependent toxicity and the distinction between safe and harmful exposure levels remain poorly established. Thus, the present study aimed to investigate the dose-dependent toxicity of AlP on biochemical biomarkers, antioxidant defense responses, and histological changes in rat liver and kidneys. Adult male Wistar rats were treated orally with increasing AlP doses (0.38, 0.58, and 1.15 mg/kg body weight, corresponding to LD50/30, LD50/20, and LD50/10, respectively) for 4 weeks. Results revealed a marked increase in body weight, serum levels of AST (aspartate aminotransferase), ALT (alanine aminotransferase), and PAL (alkaline phosphatase), and levels of urea, creatinine, and malondialdehyde (MDA) of treated rats as compared with controls. However, glutathione content and enzymatic activity of catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx), and glutathione S-transferase (GST) in liver and kidney tissue were significantly decreased compared with controls. These biochemical changes following AlP treatment also mirrored hepatic and renal histopathological observations, showing dose-dependent tissue alterations, with a more pronounced effect in the higher AlP dose-treated rats. Conclusively, sub-acute AlP exposure caused dose-dependent liver and kidney toxicity, high doses induced pronounced damage, and low doses showed mild or minimal effects.