Attenuation of Benzanthrone Toxicity by Ascorbic Acid in Guinea Pigs

Oral administration of benzanthrone (BA) (50 mg/kg body wt/day) to guinea pigs for 30 days resulted in depletion of ascorbic acid (ASA) in the liver, adrenals, and blood serum and in growth retardation (36%) and an increase (18%) in relative liver weight when compared to controls. BA treatment showed a tendency toward normocytic anemia with a decrease in hemoglobin content, reduction in RBC counts, and lowered packed cell volume. Guinea pigs treated with BA showed histopathological changes in liver including fibrosis, bile duct proliferation, and focal necrosis. Testes showed marked damage of seminiferous tubules with vacuolar degeneration and irregular and distorted interstitial spaces. BA showed evidence of patchy glomerular congestion, tubular lesions, and damaged epithelial cells in kidney, while urinary bladders had mild congestion in lamina propia and submucosa. Hepatic GOT, GPT, and LDH were found to be significantly decreased (17.5–33.5%), whereas activities of these enzymes showed a significant elevation in serum of BA-exposed guinea pigs. BA treatment also led to significant decrease of testicular hyaluronidase (29.8%) and LDH (19.8%) and significant depletion of lactic acid content (14.7%). Prior daily oral supplementation with ASA (50 mg/kg body wt) to BA-administered guinea pigs resulted in marked improvement of histopathological and biochemical changes observed in liver, testis, kidney, and urinary bladder of BA-exposed animals. These results suggest that extra supplementation of ASA could attenuate the toxic manifestations of BA.