Hesperidin ameliorates hepatic dysfunction and dyslipidemia in male Wistar rats exposed to cadmium chloride

The ever-increasing human population with attendant industrialization poses serious global health challenge. Cadmium (Cd) with other heavy metals contribute greatly to environmental pollutions and humans are daily exposed to them, leading to diverse ailments. We explored whether Hesperidin (HSP) could protect against hepatic damage and dyslipidemia in Wistar rats exposed to Cd. Forty wistar rats were randomly assigned into five groups (n = 8). Group 1 received 2 mL/kg body weight of normal saline; Group 2 received 100 mg/kg body weight of HSP while Group 3 received 5 mg/kg body weight of Cadmium Chloride (CdCl₂) for 28 days. Group 4 received 100 mg/kg body weight of HSP and after 90 min, CdCl₂ (5 mg/kg) body weight was administered for 28 days. Group 5 received 50 mg/kg body weight of HSP and after 90 min, CdCl₂ (5 mg/kg) body weight was administered for 28 days. The serum lipid profiles, hepatic dysfunction and oxidative stress markers were determined using standard methods. Cd toxicity in rats prominently elevated serum activities of AST, ALT, ALP and levels of total bilirubin, direct bilirubin, cholesterol, LDL-C and malondialdehyde with decreased levels of HDL-C, triglycerides, superoxide dismutase, catalase, glutathione and body weights. The pre-treatment of HSP before Cd intoxication prevented the dysregulated activities of liver enzymes and levels of lipid profiles, enzymatic and non-enzymatic antioxidants and other biomarkers investigated, thus suggesting anti-hyperlipidemic and hepato-protective potentials. HSP may have great potentials for development of therapeutics that could enhance the management of dyslipidemia and liver disorders associated with heavy metal exposure.