Effect of toxocara canis and trichinella spiralis infection on the activity of the mitochondrial kynurenine transaminase, the cytosolic kynurenine hydrolase and the lysosomal a-naphthyl acetate esterases in the liver of mice

In this study, the role of Toxocara canis and Trichinella spiralis infection in changing enzymatic activity that included in tryptophan metabolism via kynurenine pathway, and their effects on the activity of the lysosomal enzyme alpha-naphthyl acetate esterases, was considered. Toxocara canis and Trichinella spiralis produce a significant inhibitory effect on the kynurenine hydrolase. They produce a significant increase in the activity of the free lysosomal alpha-naphthyl acetate esterases in liver. Trichinella spiralis produces a significant inhibitory effect on the kynurenine transaminase. Larvae of the Toxocara canis parasite can remain alive releasing their metabolites in the surrounding tissues for years. As a result of this fact, the inhibitory effect of the Toxocara canis infection on the kynurenine hydrolase led to the suggestion that the accumulated kynurenine may be metabolized to 3-hydroxy kynurenine which is considered as a potent carcinogen. Nematode Trichinella spiralis inhibits kynurenine transaminase and kynurenine hydrolase and may withdraw the tryptophan and metabolize it to serotonin as well as nematode Ascaridia galli which is capable to synthesize 5- hydroxytryptamine from tryptophan via 5-hydroxy tryptophan. The increase in the activity of alpha-naphthyl acetate esterases after infection with both Trichinella spiralis and Toxocara canis larvae may be due to the increased fragility and rupture of lysosomes of the liver cells leading to the leakage of this lysosomal enzymes. Also, the rise in the enzyme activity indicates tissue damage which was attributed mostly to immunological nature. Detection of alpha- naphthylacetate esterases activity in urine and blood of patients infected with these tissue nematodes for long period should not be ignored, also detection and determination of the potent carcinogen 3- hydroxy kynurenine in urine of those patients is of urgent need

Possible lexicological hazards of some insecticides on kynurenine metabolism in mice

The objective of the present study was to investigate the in vivo effect of a single and repeated doses of some organophosphorous insecticides, Viz. Gusathione A, Dimethoate and cyolaneond some pyrethroid insecticides, Viz permethvin and AC, 227-705 commonly used in Egypt, on the liver and kidney tryptophan metabolizing enzymes: Kynurenine hydrolase KH and kynurenine aminotransferase KATE. The present study indicated that the tested insecticides caused alterations in the kynurenine metabolism with marked difference observed in the response of liver and kidney enzymes. Since these insecticides either inhibit or activate the kynurenine metabolizing enzymes, therefore we expect that exposure to these insecticides might lead to the accumulation of some tryptophan metabolites which are suspected to act as carcinogens or cocarcinogens in the process of carcinogenes is occuring in these organs

Effect of ethanol ingestion on tryptophan metabolism in streptozotocin diabetic rats.

Ingestion of ethanol by albino rats affected brain liver and plasma tryptophan contents in both normal and diabetic animals, although at different rates. Liver tryptophan was increased in both the groups, whereas tryptophan levels in brain and plasma of normal group were decreased and those of diabetic group were increased after the treatment. Similarly, while hepatic tryptophan dioxygenase activity was decreased in both the groups, activity of hepatic 3-hydroxykynureninase was increased only in normal rats and that of liver picolinic carboxylase was significantly decreased only in the diabetic group after ethanol administration.