Effects of benzo[a]pyrene on tissue activities of metabolizing enzymes and antioxidant system in normal and protein-malnourished rats

• Published in: Journal of biochemical and molecular toxicology 2003, Vol.17 (2), p.86-91
• Main Authors: Badary, Osama A., AbdEl-Gawad, Hanan M., Taha, Ragia A., Ali, Azza A., Hamada, Farid M.A.
• Format: Article
• Language: English
• Subjects: Animals; Antioxidants; Antioxidants - metabolism; Benzo(a)pyrene - toxicity; Benzo[a]pyrene; Cytochrome P-450 CYP1A1 - metabolism; Cytosol - metabolism; Diet; Environmental Pollutants - toxicity; Enzymes - metabolism; Glucuronosyltransferase - metabolism; Glutathione - metabolism; Glutathione Transferase - metabolism; Lipid Peroxides - metabolism; Liver - drug effects; Liver - enzymology; Liver - metabolism; Lung - drug effects; Lung - enzymology; Lung - metabolism; Male; Metabolising Enzymes; NAD(P)H Dehydrogenase (Quinone) - metabolism; Protein Malnutrition; Protein-Energy Malnutrition - enzymology; Protein-Energy Malnutrition - metabolism; Rat; Rats; Rats, Wistar; Stomach - drug effects; Stomach - enzymology; Stomach - metabolism; Superoxide Dismutase - metabolism
• ISSN: 1095-6670; 1099-0461
• DOI: 10.1002/jbt.10064

The effects of benzo[a]pyrene (B[a]P) on some drug‐metabolizing and antioxidant systems in liver, lung, and stomach were investigated in normal and protein malnutrition (PM) rats. PM significantly inhibited tissue glutathione (GSH) content and increased hepatic lipid peroxidation. Cytochrome P450 isoform CYP1A1 was significantly increased in various tissues (42–73%). Also, lung glutathione S‐transferase (GST) activity was significantly decreased (19%) in PM rats. On the other hand, B[a]P significantly induced tissue GSH of control and PM rats. Also, hepatic lipid peroxidation were significantly increased in control rats treated with B[a]P. Superoxide dismutase (SOD) activity was decreased by B[a]P treatment in PM rat stomach. B[a]P significantly induced both quinone reductase (QR) (in all tissues) and hepatic GST of control and PM rats. GST activity in PM rat liver was significantly higher than that of control rat liver after B[a]P treatment. Also, B[a]P induced hepatic CYP1A1 by 32‐fold and 27‐fold (P ≤ 0.05) in control and PM rats, respectively. Stomach and hepatic UDP‐glucuronosyltransferase activities were significantly decreased (34%) and increased (74%), respectively by B[a]P in PM rats. The results suggest that PM status has a modifying effect on the response of some antioxidant and metabolizing systems to a well‐known carcinogen risk. © 2003 Wiley Periodicals, Inc. J Biochem Mol Toxicol 17:86–91, 2003; Published online in Wiley InterScience (www.interscience.wiley.com). DOI 10.1002/jbt.10064