Publications by authors named "Ammigan N"

Long-term carcinogenicity studies were carried out in male Sprague-Dawley rats maintained on vitamin A-sufficient (SLO+) and vitamin A-deficient (SLO-) diets and treated with tobacco extract (TE). Three-week-old rats received by gavage a total dose of 860 mg of TE at a daily dose of 3 mg/rat over a period of 21 months. Besides tumorigenicity, drug-metabolizing phase I and phase II enzymes in lung and liver as well as vitamin A and C levels in plasma and liver were measured at 12 and 21 months of age.

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The activities of several activating enzymes and that of glutathione S-transferase as well as levels of glutathione were measured in the upper alimentary tract, lung, and liver of Swiss mice, Sprague-Dawley rats, and Syrian golden hamsters treated with 10% masheri (pyrolyzed tobacco) in diet for 20 months. Significant increase in activities of phase I activating enzymes and a remarkable decrease in the phase II detoxification system in most extrahepatic tissues of the treated animals of all three species was observed. These observations suggest that the prolonged exposure to environmental xenobiotics/carcinogens affects the drug-metabolizing enzymes of the gastrointestinal tract, which may be an important factor in determining the susceptibility of different organs to carcinogen exposure.

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Activities of several drug metabolising enzymes in the small intestine were investigated in Swiss mice, Sprague Dawley rats and Syrian Golden Hamsters fed 10% masheri, a pyrolysed tobacco product, in diet, for 20 months. The basal levels of enzymes in proximal (PI), medium (MI) and distal (DI) parts of the intestine in the three species were similar. However, the levels of cytochrome P-450, benzo(a) pyrene hydroxylase (B(a)OH) and glutathione S-transferase (GST) were highest in hamsters followed by rat and mice.

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The carcinogenicity of long-term feeding of masheri extract to animals in a vitamin-A-sufficient (SLO+) and deficient (SLO-) state was studied in Sprague Dawley rats by feeding daily dose of 3 mg extract over a period of 21 months. The phase I activating enzymes, the glutathione (GSH)/glutathione S-transferase (GST) detoxification system, and the hepatic and circulating levels of vitamins A and C were also monitored at 12 and 21 months. It was observed that the phase I enzyme activities were significantly higher in SLO+ than in SLO- rats at both 12 months and 21 months.

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The effects of N'-nitrosonornicotine (NNN) and tobacco extract on hepatic and pulmonary biotransformation enzymes were studied in rats fed vitamin A-sufficient or -deficient for semisynthetic diets. Basal levels of cytochrome P450, benzo[a]pyrene hydroxylase, benzphetamine demethylase, glutathione S-transferase and glutathione were lower in the group on the deficient diet. Treatment with tobacco extract or NNN significantly increased the levels of these enzymes in the sufficient diet group.

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The modulatory role of dietary vitamin A on the carcinogen metabolizing enzymes was studied in masheri extract and benzo[a]pyrene-treated rats. Weanling male Sprague-Dawley rats were fed vitamin A deficient (SR-) and vitamin A sufficient (SR+) semisynthetic diets for 12 weeks. ME/B[a]P treatment significantly increased the phase I activating enzymes in both SR- and SR+ groups.

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Urine samples, collected from Sprague Dawley rats treated with extracts of tobacco/masheri, benzo (a) pyrene, N'-nitrosonornicotine, N'-nitrosodiethylamine and maintained on semi-synthetic diets sufficient or deficient in Vitamin A, B and protein were tested for mutagenicity using Salmonella/microsome assay. The mutagenic activity of urine or various treated groups was in the order deficient diet greater than standard laboratory diet greater than nutritionally sufficient diet. Present results confirmed the earlier observations that nutritionally deficient animals are likely to have more exposure to mutagenic metabolites that are generated by increased phase I enzymes and decreased detoxification system.

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Studies were carried out to evaluate the changes in the phase I and II enzymes of xenobiotic metabolism, on treatment with tobacco extract (TE) and a tobacco specific carcinogen, N'-nitrosonornicotine (NNN) in Sprague-Dawley rats maintained on vitamin B complex sufficient and deficient semi-synthetic diets. Both TE and NNN significantly increased the hepatic and pulmonary phase I enzymes in the vitamin B sufficient (SB+) and deficient (SB-) animals. However, the percent increase in enzyme activities was drastically higher in the SB- treated group as compared to those in the SB(+)-treated group.

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Studies on the modulation of the carcinogen metabolizing enzymes on treatment with masheri extract (ME) and benzo (a) pyrene (B (a)P), were carried out in male Sprague Dawley rats (12 weeks old) fed a nutritionally adequate standard diet. Injection (ip) of ME and B (a) P at 3/4 LD50 dose given in 3 doses at 24 hr interval increased the phase I activating enzymes, viz. cytochrome P-450, benzo (a) pyrene hydroxylase and benzphetamine demethylase while both ME and B (a) P significantly depleted glutathione content and decreased glutathione-S transferase activity.

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The modulation of the phase I and phase II biotransformation enzymes upon treatment with tobacco extract (TE) and N'-nitrosonornicotine (NNN) was investigated using male Sprague-Dawley rats fed differential protein diets. It was observed that the animals fed a low protein diet showed an overall decrease in the basal levels of hepatic and pulmonary phase I and II enzymes. TE and NNN significantly decreased the detoxifying system in the low-protein-fed animals.

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In the present study, we report that the betel quid ingredient catechu, its extract and pure principle catechin were nonmutagenic in Salmonella typhimurium TA 100, TA 1535, TA 98, and TA 1538 assays with or without metabolic activation. They also exhibited dose-dependent decreases in mutagenicity of benzo(a)pyrene [B(a)P] and dimethylbenz(a)anthracene (DMBA) in strain TA 98 with metabolic activation. We further report that these compounds inhibited activities of cytochrome P-450 and had no effect on glutathione-S-transferase but increased the glutathione content in rat liver tissue.

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