Effect of Bendiocarb Administration on Oxidative Stress and Caspase‐3/Caspase‐9/Bax/Bcl‐2/p53 Mediated Apoptosis: The Role of Chrysin

Chrysin's effect on bendiocarb-induced oxidative stress and apoptosis was studied in a preclinical rat model. The study included 40 healthy male Wistar albino rats aged 4-6 weeks. The control group was the first of four 10-animal groups. Groups 2, 3, and 4 consisted of chrysin at a dosage of 25 mg/kg. bw, bendiocarb at a dosage of 5 mg/kg. bw, or a combination of both, by oral gavage for duration of 28 days. Blood and tissue MDA, NO, GSH, SOD, CAT, GSH-Px, GR, GST, and G6PD levels/activities were measured. Contents of glucose, triglyceride, cholesterol, BUN, creatinine, uric acid, total protein, albumin, and the activities of CPK, LDH, AST, ALT, ALP, and PChE were analyzed. A complete blood count was assayed. The animal's body/organ was weighed. Caspase-3, caspase-9, Bax, Bcl-2 and p53 protein levels of liver were measured. Bendiocarb reduced GSH, increased MDA and NO, and decreased SOD, CAT, GSH-Px, GR, GST and G6PD. Serum glucose, triglycerides, cholesterol, total protein, albumin, LDH, ALP, and PChE decreased, whereas BUN, creatinine, uric acid, CPK, AST, and ALT increased. WBC, HGB, RBC, and HCT levels dropped significantly. Although Bcl-2 decreased, liver caspase-3, caspase-9, Bax and p53 proteins increased compared to the control group. Body/organ weights dropped significantly. This study demonstrates that subchronic bendiocarb exposure induces systemic oxidative stress, biochemical dysfunction, hematological suppression, and suggesting activation of mitochondrial apoptotic pathways in rat liver. Chrysin was shown to counteract alterations in oxidative stress, apoptosis, and other parameters associated with bendiocarb exposure. In conclusion, chrysin mitigated bendiocarb-induced pathophysiological changes in the biological system.