The effect of L-tryptophan and certain other amino acids on liver nitrosodimethylamine demethylase activity.

@article{Evarts1978TheEO,
  title={The effect of L-tryptophan and certain other amino acids on liver nitrosodimethylamine demethylase activity.},
  author={R. Evarts and M. H. Mostafa},
  journal={Food and cosmetics toxicology},
  year={1978},
  volume={16 6},
  pages={
          585-9
        }
}
Summary The effect of five amino acids ( L -tryptophan, L -cysteine, L -methionine, L -tyrosine and L -glycine) on liver nitrosodimethylamine-demethylase activity was studied. Each amino acid was fed at a level of 1% of the diet to weanling male Wistar rats for 12 days. Tryptophan increased the enzyme activity and cysteine had the opposite effect. The other amino acids tested had no effect. When the effect of the duration of the tryptophan feeding (3–47 days) and the age of the animals (21–51… Expand
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References

SHOWING 1-10 OF 33 REFERENCES
The effect of cysteine on the metabolic changes produced by two carcinogenic Nnitrosodialklamines in rat liver.
TLDR
It is concluded that both the toxic and the carcinogenic effects of the N-nitrosodialkylamines are due to the in situ formation of diazoalkanes, which are alkylating agents and appear to interact primarily with the endoplasmic reticulum of the liver cells. Expand
STUDIES ON THE INDUCTION AND REPRESSION OF ENZYMES IN RAT LIVER. 3. INDUCTION OF ORNITHINE DELTA-TRANSAMINASE AND THREONINE DEHYDRASE BY ORAL INTUBATION OF FREE AMINO ACIDS.
TLDR
The present investigation was designed to determine whether or not a degree of specificity exists in the dietary amino acid requirements for the induction of threonine dehydrase and ornithine transaminase. Expand
Counteraction by sulphydryl compounds of the enzymic conversion of and the metabolic lesions produced by two carcinogenic N-nitrosodialkylamines in rat liver
Abstract (1) The in vivo and in vitro effects of various sulphydryl compounds on the metabolic conversion (N-dealkylation) of the N-nitrosodialkylamines, DMNA∗ and DENA, to their toxic and suspectedExpand
Effect of l-tryptophan on diethylnitrosamine and 3'-methyl-4-n-dimethylaminoazobenzene hepatocarcinogenesis.
TLDR
Tryptophan decreased the incidence of liver tumours in bothDENA- and 3′-MeDAB-fed animals but had no effect on the location and incidence of oesophageal tumours among DENA- fed animals. Expand
Toxicity and metabolism of drugs in relation to dietary protein.
TLDR
The purpose of present study is to investigate the effect of high and low protein diet on the toxicities of various drugs in relation to the drug-metabolizing activities of liver microsomes, and to investigate whether the alternation in theDrugs may be correlated to the activities of microsomal NADPH-linked electron transport system. Expand
Amino acid induction and carbohydrate repression of dimethylnitrosamine demethylase in rat liver.
TLDR
It is suggested that starvation-induced increase is due to de novo protein synthesis, consistent with the observed increase in maximal velocity, and the level of dimethylnitrosamine demethylase in liver is under the control of multiple regulatory factors. Expand
Effect of protein deprivation of male weanling rats on the kinetics of hepatic microsomal enzyme activity.
TLDR
It is suggested that the diminution of enzyme velocities for the low protein group is related both to a lower DNA content per gram tissue and to a loss of specific enzymic activity per milligram microsomal protein. Expand
Enhancement of urinary bladder tumorigenesis in hamsters by coadministration of 2-acetylaminofluorene and indole.
TLDR
Adding indole or tryptophan protected the liver from AAF injury and greatly reduced the development of cholangiocarcinomas in hamsters. Expand
The effect of oral phenobarbitone on hepatic microsomal cytochrome P-450 and demethylation activity in rats fed normal and low protein diets.
TLDR
A 0.1% solution of sodium phenobarbitone instead of normal drinking water causes maximal stimulation of enzyme activity and an increase in cytochrome P-450, of 7-fold over controls; there are also increases in liver weight and microsomal protein. Expand
Effects of dietary protein quality on drug metabolism in the rat.
TLDR
Increase in drug metabolism by PB was accompanied by a parallel rise in microsoinal protein and cytochrome P-450 with group 2 animals exhibiting relatively higher levels than group 1. Expand
...
1
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3
4
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