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Departments of Nutrition and Home Economics, Cook College, Rutgers University, New Brunswick, NJ 08903
Oxidation of tryptophan and urinary excretion of N1-methylnicotinamide were studied in rats fed a modified DeCarli-Lieber liquid diet of low (1.1 mg/liter or 5 mg/kg dry diet) and adequate (5.5 mg/liter or 25 mg/kg dry diet) nicotinamide content with and without ethanol replacing carbohydrate to 36% of total calories. Protein was restricted to 12% of calories so that the tryptophan content was about 0.16% of dry weight. Rats were fed for 30 or 40 days and feeding was restricted to 7 or 12 hours per day. N1-Methylnicotinamide was measured in urine collected during the last 2 days of feeding. At the end of the experimental period, fasted rats were injected intraperitoneally with 0.8 µCi of L-[ring-2-14]tryptophan (0.12 or 0.11 µCi/mg tryptophan) or 0.7 µCi of[14C]formate (0.44 µCi/mg formate) per 100 g body weight. Expired CO2 was collected every 30 minutes or hourly for 5 or 6 hours. N1-Methylnicotinamide excretion was increased in ethanol-fed rats (P < 0.05). The percent of injected [14C]tryptophan recovered as 14CO2 was increased in rats fed ethanol in a low niacin diet as compared to controls (P < 0.01). Recovery of 14CO2 from [14C]formate oxidation was not affected by ethanol feeding. These findings suggest that the initial oxidation of tryptophan by tryptophan 2,3-dioxygenase is enhanced following chronic ethanol feeding.
KEY WORDS: tryptophan tryptophan oxygenase nicotinamide chronic ethanol feeding
1 This research was supported by Biomedical Sciences Research Grants, Rutgers University.
2 Send reprint requests to: Dr. J. I. Patterson, Department of Home Economics, Cook College, Rutgers University, New Brunswick, NJ 08903.
Manuscript received 22 December 1982.