Evaluation of the Ameliorative Impact of ß, Epsilon-Carotene-3, 3’-diol on the Hepatic System after Ethanol-influenced Liver Toxicity in Adult Male Wistar Rats: Morphological and Biochemical Analyses

The frequency of liver injury is rising universally due to the leisure and societal acceptance of ethanol (EtOH) consumption. Enzymes that break down ethanol are primarily found in the liver, as such, the effects of long-time ethanol drinking cause a more serious effect on the liver as opposed to other body parts like the heart, brain, and gastrointestinal organs. Ethanol-induced hepatic injury occurs through oxidative stress, lipid accumulation, and inflammation. This experiment was carried out to investigate the impacts of ß, ?-Carotene-3,3’-diol on the hepatotoxicity induced by EtOH in Wistar rats. A total of 48 Wistar rats were purchased and randomly split into six distinct groups (n=8): Oral administration was carried out using oral cannula. The control group was Group A, Group B = EtOH-only, and Group C = EtOH, + ß, Epsilon-Carotene-3,3’-diol at 10 mg/kg, group D = EtOH, + ß, Epsilon-Carotene-3,3’-diol at 20 mg/kg, group E = EtO.H, + ß, Epsilon-Carot.ene-3,3’-diol at 40 mg/kg, and group F = EtOH + Silymarin 200 mg/kg. At sacrifice, blood samples were collected to determine antioxidant activity by assaying for superoxide dismutase (SOD), and catalase. The total protein level, malondialdehyde and the concentration of tumor necrosis factor-alpha (TNF-?) was evaluated for the effects of EtOH on inflammation and lipid peroxidation. The results showed ethanol caused macrovesicular and microvesicular steatosis. EtOH caused an increase in MDA and TNF-? concentration, and a reduction in catalase, SOD, and TP level. Remedy with ß, Epsilon-Carot.ene-3,3’-diol after ethanol-influenced hepatoxicity highlights its ameliorative ability in a dose-reliance pattern.

Key Words: alcoholic liver disease, ethanol, hepatotoxicity, ß, ?-Carotene-3,3’-diol, hepatocellular ballooning