Authors: Timothy O. Oni, Iboyi Nathaniel Onuche, Dokubo Chinweike Unoma, Odo Vincentmary C, Kene-Okonkwo Adachukwu, Iboko Ifeoma Juliet
Abstract: Alcohol (ethanol) is a hepatotoxic agent that induces oxidative stress and disrupts liver function. This study evaluated the effects of three commercial ethanol brands (Seaman, Chelsea, and Lords) at high (3 ml/kg/day) and low (1.5 ml/kg/day) doses on liver function and antioxidant status in Wistar rats. Thirty-five rats (150–160 g) were divided into seven groups (n = 5) and treated for two weeks. Liver enzymes (ALT, AST), protein profile, bilirubin, and oxidative stress markers (SOD, CAT, LDH, MDA) were analyzed using standard methods. Control values were ALT = 24.26 U/L and AST = 138.23 U/L. High-dose Seaman produced the greatest hepatotoxicity (ALT = 39.33 U/L; AST = 203.53 U/L), followed by Lords (ALT = 32.23 U/L; AST = 156.33 U/L), while Chelsea reduced AST (101.66 U/L). Albumin decreased markedly in Seaman high-dose (1.23 g/dL vs. 2.22 g/dL control). Oxidative markers showed SOD = 27.01 ×10⁻⁶ U/mL and CAT = 88.02 U/mL in controls. Lords low-dose caused severe depletion (SOD = 6.63 ×10⁻⁶ U/mL), while Chelsea high-dose increased antioxidant activity (SOD = 43.11 ×10⁻⁶ U/mL; CAT = 122.73 U/mL) but elevated LDH (489.75 μg/mL). Ethanol induced dose- and brand-dependent hepatotoxicity. Seaman was most hepatotoxic, Lords caused greatest oxidative depletion, while Chelsea elicited adaptive antioxidant responses with cellular damage.
DOI: http://doi.org/10.5281/zenodo.20134138
