Relative modulatory potential of quercetin, catechin, silymarin and genistein on cellular antioxidant system and liver histology during gentamicin-induced acute toxicity in rats

• Modulation of GEN-induced hepatotoxicity by phytochemicals was studied in rats. • Phytochemicals attenuated plasma biomarkers, antioxidant status and histopathological lesions in the affected liver. • Quercetin, silymarin, catechin and genistein coadministration improved the hepatic antioxidant system. • Silymarin and quercetin were more effective in reducing hepatic dysfunctions induced by GEN. The study aimed to determine the modulatory potential of different phytochemicals (quercetin, catechin, silymarin and genistein) on the hepatic antioxidant system and histology during acute toxicity induced by gentamicin (GEN) in rats. Adult Wistar rats ( n = 66) were randomly allocated to eleven groups. Administration of GEN increased ( p < 0.05) plasma activities of AST, ALT, GGT and ALP in a dose-dependent manner, indicating acute hepatic dysfunctions in rats. It also increased ( p < 0.05) levels of malondialdehyde (MDA) and advanced oxidation protein product (AOPP) in hepatic tissues and reduced total antioxidant status (TAS), total thiols (TTH), reduced glutathione (GSH), glutathione reductase (GR), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase (CAT) activities, indicating intensity of hepatic damage. These observations accompanied various histopathological changes such as infiltration of inflammatory cells in the vicinity of severely atrophied hepatocytes, degenerative changes, vacuolar degeneration or complete loss of parenchyma in the liver in a dose-dependent manner. The concurrent exposure of phytochemicals along with GEN significantly ( p < 0.05) reduced hepatic tissue damage as indicated by reduced levels of MDA and AOPP in hepatic tissue and improved hepatic antioxidant system and hepatocellular architecture. Overall, silymarin and quercetin showed better effects than catechin and genistein in reducing hepatic dysfunctions induced by GEN in rats.