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Biomedical subjects

C Gopinath

Publications and source records attributed to C Gopinath.

At least 55 records · Page 3Linked to original sources
PubMed1975

Experimental chronic copper toxicity in sheep. Changes that follow the cessation of dosing at the onset of haemolysis.

Eight sheep were given daily oral doses of copper sulphate until haemolysis occurred. Three of the sheep developed further periods of haemolysis after dosing ceased. Serum enzyme and urea levels were measured throughout the experiment and compared to those obtained from three undosed control sheep. Serum enzyme levels rose prior to haemolytic crises and urea levels rose subsequent to haemolysis in animals that died or were killed in extremis. Severe morphological changes were seen in liver, kidney and brain. Tissue levels of copper and iron were markedly elevated. It is concluded that tissue damage continues even after the cessation of ingestion of copper and that the damage can be severe enough to lead to repeated haemolytic crises.

Alcohol Oxidoreductases↗
PubMed1975

A comparative enzyme histochemical and histological study of the effect of ischaemia and post mortem change on rat kidneys.

A histochemical study of the effect of ischaemia on rat kidneys showed that changes were demonstrable in adenosine triphosphatase, alkaline phosphatase and succinic dehydrogenase within 2 h. Further changes occurred with increasing time. The activity of acid phosphatase was little affected up to 24 h although at this time there was marked tubular disruption. Paraffin embedded H and E sections also showed marked changes within 2 h. Enzyme histochemical and histological changes in kidneys taken at varying periods after the death of the animal showed very similar changes to those in ischaemic kidneys. Differences were mainly in the rate and extent of the changes.

Acid Phosphatase↗
PubMed1975

The role of microsomal hydroxylases in the modification of chloroform hepatotoxicity in rats.

Male rats have a greater microsomal amidopyrine N-demethylase activity per unit weight of liver, a shorter hexobarbitone sleeping time and are more susceptible to the hepatotoxic effect of chloroform than female rats. Phenobarbitone sodium, phenylbutazone and DDT induce microsomal amidopyrine N-demethylase in the liver of the male rat and reduce hexobarbitone sleeping time. Chlorpromazine is less effective in this respect. Phenobarbitone, phenylbutazone and, to a lesser extent, chlorpromazine potentiate the hepatotoxic effect of chloroform in male rats. SKF 525A, sodium diethyl-dithiocarbamate and carbon disulphide increase hexabarbitone sleeping time in male rats and protect to varying degrees against the hepatotoxic effect of chloroform.

Animals↗