[Effects of ingestion of an antioxidant, BHT, on the metabolism of ascorbic acid and vitamin A in rats]. / Effets de l'ingestion d'un antioxygène alimentaire, le B.H.T., sur le métabolisme de l'acide ascorbique et de la vitamine A chez le rat.

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.

[Metabolism of nucleic acids in testicles of adult rats deficient in vitamin A]. / Métabolisme des acides nucléiques dans le testicule de rat adulte carencé en vitamine 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).

[Effects of ascorbic acid deficiency on lactate dehydrogenase. Quantitative and isoenzymatic study]. / Conséquence de la carence en acide ascorbique sur la lacticodéshydrogénase. Etude quantitative et isoenzymatique

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.

[Nucleic acid metabolism in testes from adult rats deficient in vitamin A]. / Quelques aspects du métabolisme nucléique dans les testicules de Rat adulte carencé en vitamine A

Our study related to degenerescence of testes in vitamin A deficient rats led to the following observations : decrease of DNA, RNA on one hand and AMP, ADP and ATP on the other hand. These observations are considered as related to decrease of DNA polymerase activity.

[Biochemical aspects of testicular degeneration in the vitamin A deficient rat. 4. Permeability of the vascular walls]. / Aspects biochimiques de la dégénérescence testiculaire du rat carencé en vitamine A. IV. Perméabilité des parois vasculaires

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.