Effect of combined deficiency of fat and vitamin A on N-nitrosodiethylamine-induced lung carcinogenesis in mice

Khanduja, Krishan Lal; Koul, Indu Bala; Gandhi, Rajinder Kaur; Sehgal, S; Sharma, Rahul

doi:10.1016/0304-3835(92)90198-5

Cited by 2 publications

(3 citation statements)

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“…B[a]P is a representative polycyclic aromatic hydrocarbon with well-documented carcinogenic properties [23]. The carcinogenic potential of B[a]P not only varies between species, but also depends on several physiological and environmental variables [2,11]. Among these factors, protein deficiency is known to alter various drug-metabolising enzymes and antioxidantdefense system [24,25].…”

Section: Discussionmentioning

confidence: 99%

“…Genetic and environmental factors contribute to a wide inter-and intraindividual variability in drug metabolism and hence carcinogenicity. Among the environmental factors that may interfere with B[a]P metabolism, the diet and nutritional status of individuals are important determinants [2,3].…”

Section: Introductionmentioning

confidence: 99%

“…Alterations in drug-metabolizing enzymes and glutathione (GSH)-dependent metabolism are being used to monitor the toxicity of various xenobiotics and toxicants [10,11]. While there are sufficient studies on the effect of nutrient deficiencies, such as vitamin A [2] and riboflavin [12], on B[a]P-metabolising enzymes and cacinogenicity, no studies are, however, available on the impact of protein malnutrition (PM). In this paper, we report our findings on B[a]P metabolising and antioxidant enzymes in selected tissues of rats that were subjected to experimental PM.…”

Section: Introductionmentioning

confidence: 99%

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

Badary

Abd-ElGawad

Taha

et al. 2003

J Biochem & Molecular Tox

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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 < or = 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.

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