Biomedical subjects

D Gripois

Publications and source records attributed to D Gripois.

50 records · Page 3Linked to original sources

PubMed1979

[Enzymatic N-acetylation of tryptamine by brain homogenates of Locusta migratoria before and after intoxication by chlordimeform or lindane (author's transl)].

Brain homogenates of Locusta migratoria are found to possess enzyme capable of catalyzing the N-acetylation of tryptamine. A main product of the enzymatic reaction is isolated and identified as N-acetyltryptamine by chromatography analyse. Both insecticides, chlordimeform and lindane, inhibit enzyme activity. A direct correlation between the degree of intoxication and acetylation of tryptamine is described.

Acetylation↗

PubMed1977

[Monoamine oxidase activity of the brain of Locusta migratoria in normal conditions and after intoxication by two insecticides: chlordimeform and dieldrin].

Our investigations have shown up an MAO activity in locust brain, by the use of a radio-isotopic method, as much at larval as at adult stage. This MAO activity is in a sample of 34,3 dpm/mg of brain tissue (wet weight). Investigations have also been undertaken on effects of dieldrin and chlordimeform poisoning on this MAO activity. Even at sublethal dosages, chlordimeform causes a significant inhibition of MAO activity in vivo. This finding is in accordance with Beeman and Matsumura's work in vitro. Moreover, acute poisoning by dieldrin produces more than 60% of inhibition of MAO, 3 hours after administration of 115 microng of this insecticide by injection in the hoemocelian cavity.

Amidines↗

PubMed1977

Effects of thyroid hormones on the evolution of monoamine oxidase activity in the brain and heart of the developing rat.

The evolution of monoamine oxidase (MAO) activity towards tryptamine has been studied from birth to 20 days post-natal in the brain and heart of male rats. Hyperthyroidism was induced by thyroxine injections and hypothyroidism by PTU administration. The results are expressed per unit of fresh weight and per unit of protein weight. Cardiac MAO is higher in the hyperthyroid animals than in controls as soon as 5 days following birth; the difference between the 2 groups increases until 20 days. The deficiency in thyroid hormones, on the other hand, was followed by a slight decrease in the cardiac enzyme, this decrease reflecting the general deficit in protein synthesis. Brain MAO is not affected by hyperthyroidism, but a clear deficit follows PTU administration. This deficit is significant beginning at 10 days and the difference between the 2 groups increases up to 20 days. The effects of PTU-induced hypothyroidism can be corrected by thyroxine injections. Except for the decrease in the level of cardiac enzyme in hypothyroid animals, all the effects on MAO activity are independent of the total protein content of both organs.

Animals↗

PubMed1976

[Influence of thyroid hormones on monoamine oxidase activity in newborn rats].

In young Rats made hypothyroid from birth, the activity of monoamine oxidase at 20 days is smaller than controls in brain, heart and kidney. In Rats made hyperthyroid by injections of thyroxine, the activity is lower in brain kidney and liver and is 3.8 times higher in the heart.

Animals↗

PubMed1975