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Biomedical subjects

K Majumdar

Publications and source records attributed to K Majumdar.

7 recordsLinked to original sources
PubMed1981

Replication of DNA in larval salivary glands of Drosophila after in vivo synchronization.

The replication of DNA in the giant chromosomes in different cells of Drosophila larval salivary glands is asynchronous. A method of in vivo synchronization of the nuclei has been successfully devised by a 5'-fluorodeoxyuridine (FdU) block-release-thymidine chase technique, and the patterns of replication sequences have been examined by 3H-thymidine autoradiography. When the larvae of Drosophila melanogaster are fed on FdU for 48 h, and the block is released thereafter, most cells are found in mid-replication phase (termed 3C). When the larvae are subjected to a chase in normal Drosophila medium (or sucrose), a series of cells arrive at 3C phase about every 8 h. When they are chased in sucrose containing thymidine, the number of cells in 3C phase rises to 70%, and then drops rapidly to 1-2% of all labelled cells. The terminal phases (3D, 2D and 1D) reach a peak between 4-8 h. At 12-14 h of chase the 3D-1D peaks decline and a third peak consisting mostly of the initial phases (DD-1C) is found at 14--16 h. The replication of DNA in polytene chromosomes of Drosophila thus seems to proceed in a regular sequence of DD-3C-1D.

Animals↗
PubMed1979

Biochemical studies on nickel toxicity in weanling rats -- influence of vitamin C supplementation.

The influence of high intake of vitamin C in the young growing rats under administration of nickel sulphate in toxic doses has been studied. Ingestion of nickel sulphate depresses the growth rates of rats, alters the vitamin C status in different tissues, inhibits certain enzymes of vitamin C metabolism and changes the activities of alkaline phosphatase and succinic dehydrogenase in the liver and kidney tissues. The acid phosphatase activity of liver, kidney and brain tissues of rats and glucose-6-phosphatase activity in liver, and serum GOT activity were stimulated, with reduction in the in the liver GOT activity. There is stimulation in the activities of rat brain inorganic pyrophosphatase and cholinesterase. Kidney tissues of rats were found to be more susceptible towards nickel toxicity as compared to the hepatic tissues in respect of morphological alterations. There is almost no alteration in the hepatic lipid composition. Administration of vitamin C in high doses to rats fed nickel salts in toxic doses can restore not only the growth rates but also certain enzyme activities to a significant extent.

Acid Phosphatase↗
PubMed1978

Studies on L-ascorbic acid metabolism in rats under chronic toxicity due to organophosphorus insecticides: effects of supplementation of L-ascorbic acid in high doses.

The effects of chronic administration of two organophosphorus insecticides, parathion and malathion on the growth rate, ascorbic acid metabolism and some other nutritional and physiological parameters in rats were studied. Both parathion and malathion toxicity retarded the growth rate of rats. Inhibition of brain acetylcholinesterase was taken as an index of organophosphorus insecticide toxicity. Haemoglobin concentration of blood and organ weights were not affected under the toxic conditions. Parathion and malathion administration stimulated the activity of L-gulonolactone oxidase along with a simultaneous increase in the tissue storage and urinary excretion of vitamin C. The activities of other enzymes of ascorbic acid metabolism, dehydroascorbatase, uronolactonase, and L-gulonate dehydrogenase and decarboxylase were altered under the experimental conditions. Only minor histological changes of the liver and kidney tissues were noted under parathion and malathion toxicities. Excess intake of vitamin C under the toxic conditions was found to be very effective in counteracting the growth retardation and also the alterations produced by parathion and malathion both at the enzymatic and histological levels.

Animals↗
PubMed1978

Biochemical studies on polychlorinated biphenyl toxicity in rats: manipulation by vitamin C.

The effects of chronic polychlorinated biphenyl (PCB) compound toxicity on L-ascorbic acid metabolism in rats have been studied. PCB treatment brought about a depression in the activities of the enzymes L-gluonolactone oxidase and dehydroascorbatase along with an increased tissue levels and urinary excretion of L-ascorbic acid. PCB toxicity drastically disturbed the normal histological pattern of the liver cells and also significantly changed the hepatic lipid composition. L-ascorbic acid supplementation to the toxicated group of animals, although could not prevent the growth retardative effect of PCB, could afford a definite protection against the enzyme activity alterations and histological changes as caused by PCB toxicity.

Alcohol Oxidoreductases↗
PubMed1977

Effects of chronic vanadium pentoxide administration on L-ascorbic acid metabolism in rats: influence of L-ascorbic acid supplementation.

1. Rats toxicated with vanadium pentoxide showed drastic retardation in growth rate and supplementation of L-ascorbic acid to these rats could not reverse this effect. The urinary excretion of L-ascorbic acid and D-glucuronic acid was decreased in the toxicated group of rats. 2. Considerable lowering of L-ascorbic acid content of the liver tissues of rats was observed under vanadium toxicated conditions. Supplementation of L-ascorbic acid to this group raised the tissue Vitamin C reserve considerably. 3. The normal histological patterns of the liver and kidney tissues of rats were severely disturbed under vanadium toxicated conditions. L-ascorbic acid supplementation to this group of rats showed marked signs of restoration in this respect. 4. Vanadium pentoxide treatment brought about a significant reduction in the biosynthetic capacity of L-ascorbic acid, along with an enhanced utilization of this vitamin. Subsequent supplementation of L-ascorbic acid to the toxicated group of rats was found to be effective in reversing these effects almost to the basal level.

Animals↗