ATTENUATION OF BENZANTHRONE TOXICITY BY ASCORBIC-ACID IN GUINEA-PIGS

Oral administration of benzanthrone (BA) (50 mg/kg body wt/day) to gui nea pigs for 30 days resulted in depletion of ascorbic acid (ASA) in t he liver, adrenals, and blood serum and in growth retardation (36%) an d an increase (18%) in relative liver weight when compared to controls . BA treatment showed a tendency toward normocytic anemia with a decre ase in hemoglobin content, reduction in RBC counts, and lowered packed cell volume. Guinea pigs treated with BA showed histopathological cha nges in liver including fibrosis, bile duct proliferation, and focal n ecrosis. Testes showed marked damage of seminiferous tubules with vacu olar 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 co ngestion in lamina propia and submucosa. Hepatic GOT, GPT, and LDH wer e found to be significantly decreased (17.5-33.5%), whereas activities of these enzymes showed a significant elevation in serum of BA-expose d guinea pigs. BA treatment also led to significant decrease of testic ular hyaluronidase (29.8%) and LDH (19.8%) and significant depletion o f lactic acid content (14.7%). Prior daily oral supplementation with A SA (50 mg/kg body wt) to BA-administered guinea pigs resulted in marke d improvement of histopathological and biochemical changes observed in liver, testis, kidney, and urinary bladder of BA-exposed animals. The se results suggest that extra supplementation of ASA could attenuate t he toxic manifestations of BA. (C) 1994 society of Toxicology.