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Biomedical subjects

T Terroine

Publications and source records attributed to T Terroine.

At least 19 recordsLinked to original sources
PubMed1979

[Effects of ingestion of an antioxidant, BHT, on the metabolism of ascorbic acid and vitamin A in rats].

The antioxidant foor additive, BHT, was fed to male rat for 28 days at a 0.5% concentration in a diet containing ascorbic acid or not. BHT intake had no effect on ascorbic and dehydroascorbic acid contents in the adrenals, spleen or liver, whether or not the diet contained ascorbic acid. When the ration included 100 mg/kg of ascorbic acid, BHT intake caused a sharp rise in urinary excretion of this compound. This data confirm the work of other authors studying an ascorbic acid-poor diet. These results indicate that BHT intake leads to increased synthesis of ascorbic acid. This augmentation would be the result of stimulating the biosynthesis pathway of uridyl-di-phospho-glucuronic acid, which is necessary to the elimination of BHT in the form of glucuroconjugate. BHT intake in an ascorbic acid-rich diet reduces hepatic vitamin A concentration by 44 p. 100 and the hepatic reserve of this vitamin by 22 p. 100. BHT detoxication, as that of other exogenous compounds, thus seems to cause increased vitamin A utilization.

Adrenal Glands↗
PubMed1976

[Metabolism of nucleic acids in testicles of adult rats deficient in vitamin A].

Avitaminosis A, applied on deficient rats receiving retinoic acid leads to an important decrease of thymidine incorporation in testicular DNA in vivo as well as in vitro. On the contrary uridine incorporation in RNA is considerably increased in vitro as well as in vivo. The function of ribosomes, as measured by the aggregation ability in the polysomes, is not altered by vitamin A deficiency. From these results one can say that the degenerescence of rat testicle is accompagnied by a decrease of DNA anabolism and a stimulation of RNA anabolism due to an increase of its catabolism (compensatory synthesis).

Animals↗
PubMed1976

[Biochemical aspects of testicular degeneration in the vitamin A deficient rat. 4. Permeability of the vascular walls].

Vitamin A deficiency modifies Na and K concentration values in oedematous testes. On one hand there is an increase of Na, on the other hand a decrease of K. Subcellular protein concentrations are impaired. Testicular fluid electrophoresis show it gets from plasma or lymph. No significant influence of ATPase (Na,+ K+) was demonstrable. Stimulation of lysosomal beta-glucuronidase can explain this fluid accumulation.

Adenosine Triphosphatases↗
PubMed1975

[Effects of ascorbic acid deficiency on lactate dehydrogenase. Quantitative and isoenzymatic study].

Light, acute vitamin C deficiency or repletion had no uniform effect on lactiodeshydrogenase, each organ reaching specifically (skeletal muscle, heart, kidney, spleen, liver adrenals, testes). There was no correlation with the age of the animal except in the case of testicular lacticodeshydrogenase isoenzymes. Reduction of food intake caracteristic of the late state of scurvy had no effect on the distribution of isoenzymes which was also independent of quantitative variations of enzyme activity. Vitamin C repletion restored the normal distribution of isoenzymes in spleen and liver but not in skeletal muscle. In the last phase of acute vitamin C deficiency, lactiodeshydrogenase activity was generaly elevated (heart and skeletal muscle excepted). When ascorbic acid was given back lacticodeshydrogenase activity remained elevated in liver and spleen but was lowered in skeletal muscle.

Acute Disease↗