Crocin alleviates lead acetate-induced liver and kidney damage in rats by regulating oxidative stress, autophagy, apoptosis, and histopathological changes.

Lead (Pb) is a heavy metal that can trigger oxidative stress, causing toxic effects particularly on the liver and kidneys. Crocin (Cro) has been demonstrated to possess anti-autophagic and anti-apoptotic properties in addition to its antioxidant activity. The objective is to assess Cro's capacity to stop Pb-induced liver and kidney damage. A total of 32 rats were used in the investigation, split into four groups of eight rats each: Control, Cro, PbAc, and PbAc + Cro. In addition to histopathological improvement, treatment with Cro (50 mg/kg, orally, for 7 days) alleviated the damage to liver and kidney tissues caused by PbAc (30 mg/kg, orally, for 7 days) by reducing levels of ALT, AST and ALP, as well as blood urea and creatinine. Cro treatment also increased GSH levels, SOD and CAT enzyme activities and lowered MDA levels in PbAc-induced tissues. By raising 8-OHdG levels in liver and kidney tissues, PbAc damaged DNA. It also stimulated autophagy by elevating Beclin-1, LC3A, and LC3B levels. In addition to all this, it activated apoptosis by increasing Bax and Cyt-c levels whilst reducing Bcl-2 synthesis. However, treatment with Cro decreased DNA damage, autophagy, and apoptosis in both tissues. Our results suggest that Cro could be able to lessen the adverse effects of PbAc-induced liver and kidney damage.