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Biomedical subjects

K Subrahmanyam

Publications and source records attributed to K Subrahmanyam.

At least 19 recordsLinked to original sources
PubMed1991

Ultraviolet light-induced unscheduled DNA-synthesis in isolated neurons of rat brain of different ages.

DNA-repair capacity, by incorporation in vitro of [3H]thymidine into DNA of isolated neuronal cells and splenic lymphocytes of rat was studied as a function of age. The incubations were carried out both in the presence and absence of hydroxyurea (HU), a known inhibitor of replicative DNA synthesis. The results indicate that neurons, unlike lymphocytes, obtained from adult and old animals offer a good model system to measure the DNA-repair process without any possible interference of DNA replicative synthesis. Further, the 'spontaneous' DNA repair by unscheduled DNA synthesis (UDS) in old neurons remained unchanged as compared to the adult level. However, the response of aging neurons, in contrast to that of young and adult neurons or of lymphocytes of any age, to a mutagenic challenge like UV light is limited. It is suggested that this lack of responsive DNA-repair against a given damage may lead to a general metabolic deterioration and senescence.

Aging↗
PubMed1990

Substrate-affinity relation of succinate and lactate dehydrogenases in tissues of toad, Bufo melanostictus under electropolarity treatment.

The kinetic analysis of succinate and lactate dehydrogenases (SDH and LDH) has been studied in muscle and liver of Bufo melanostictus under electropolarity treatment. Increased Vmax and decreased Km were observed both in liver and muscle under cathode electropolarity treatment whereas a reverse trend was noticed under anodal treatment. But the activation energy values (delta E) of both the enzymes decreased indicating enhanced catalytic efficiency under both cathodal and anodal treatments.

Animals↗
PubMed1988

On the type of DNA polymerase activity in neuronal, astroglial, and oligodendroglial cell fractions from young, adult, and old rat brains.

DNA polymerase activity in isolated neuronal, astroglial, and oligodendroglial cell-enriched fractions from rat brains of different ages was measured. Attempts were made to distinguish the total activity into beta and alpha polymerase types making use of inhibitors like ddTTP and aphidicolin. The results indicate that at all the ages studied (16th day embryonic and 1, 225, and greater than 540 days postnatal), neurons possess the highest polymerase activity in comparison with other types of cells. Further, throughout the postnatal life the polymerase present in neuronal cells is of the beta type and this activity remains fairly constant from adult to old age. In contrast, both astroglial and oligodendroglial cells at adult and old stages of life appear to possess other type(s) of polymerase activity in addition to the predominant beta polymerase. It is inferred that neurons, being postmitotic, are equipped with efficient DNA-repair machinery throughout their life span.

Age Factors↗
PubMed1985

Functional relationship of ammonia to DNA, RNA and protein in brain.

The functional significance of the production of ammonia during neuronal activity is not known, although a number of studies are available concerning the mechanism of of ammonia toxicity in brain. Hyperammonemia without behavioural change was induced in experimental rats by i.p. administration of either a single dose of ammonium acetate or 6 doses with an interval of 1 h during the day or one single dose daily for 7 days. No significant change was observed in the content of DNA, RNA and protein in cerebral cortex, cerebellum and brain stem following the administration of a single dose. There was a marked decreased in the content of DNA in all three brain regions after the administration of 6 hourly doses of ammonium acetate. Under these conditions the RNA was found to increase in all three brain regions. A decrease in the content of protein per gram wet weight was observed in cerebral cortex and brain stem while the change in cerebellum was found to be insignificant. However, the content of RNA and protein was found to show a very significant increase when expressed per microgram of DNA for each region under these conditions, indicating an increase in RNA and protein in the cells surviving the toxic damage caused by ammonia. A marked and significant increase in the content of RNA and protein was observed in all three brain regions following the administration of a single dose per day for 7 days. These results are discussed not only with respect to toxic damage to the glial cells by ammonia, but also with respect to the probable effect of ammonia liberated during neuronal activity on inhibition of lysosomal degradation of protein, and on its stimulatory effects of transcriptional and translational activities. The increased RNA and protein under these conditions may be contributing not only in the proliferation of glial cells (Alzheimer Type II cells) but also in the dendritic spinous growth.

Acetates↗
PubMed1972

Evaluation of the rate-limiting steps in the pathway of glucose metabolism in kidney cortex of normal, diabetic, cortisone-treated and growth hormone-treated rats.

1. The activities of gluconeogenic and glycolytic enzymes and the concentrations of citrate, ammonia, amino acids, glycogen, glucose 6-phosphate, acetyl-CoA, lactate and pyruvate were measured in kidney cortex of normal, diabetic, cortisone-treated and growth hormone-treated rats. 2. In kidney cortex of diabetic, cortisone-treated and growth hormone-treated rats the activities of glucose 6-phosphatase (EC 3.1.3.9), fructose 1,6-diphosphatase (EC 3.1.3.11) and phosphopyruvate carboxylase (EC 4.1.1.32) were increased. 3. The activities of glutamate dehydrogenase (EC 1.4.1.3), alanine aminotransferase (EC 2.6.1.2), aspartate aminotransferase (EC 2.6.1.10) and pyruvate carboxylase (EC 6.4.1.1) were increased in diabetic and cortisone-treated rats. In growth hormone-treated rats the activity of aspartate aminotransferase was depressed but those of the other three enzymes were unchanged. 4. The activity of hexokinase (EC 2.7.1.1) was not altered in any of these conditions. Phosphofructokinase (EC 2.7.1.11) activity was depressed only in growth hormone-treated rats. Pyruvate kinase (EC 2.7.1.40) activity was depressed in cortisone-treated and growth hormone-treated rats but unchanged in diabetic rats. 5. Amino acids, acetyl-CoA and glucose 6-phosphate contents were increased in rat kidneys in all these three conditions. Ammonia content was increased in diabetic and cortisone-treated rats but was markedly diminished in growth hormone-treated rats. 6. The [lactate]/[pyruvate] ratio was elevated in diabetic and cortisone-treated rats but unchanged in growth hormone-treated rats. Citrate content was increased in the kidney cortex of diabetic and growth hormone-treated rats but was unchanged in cortisone-treated rats. The activity of ATP citrate lyase (EC 4.1.3.8) was depressed in diabetic and growth hormone-treated rats but was increased in cortisone-treated rats. 7. Glycogen content was moderately elevated in growth hormone-treated rats and markedly elevated in diabetic rats, whereas no change in glycogen content was observed in cortisone-treated rats. Glycogen synthetase (EC 2.4.1.11) activity was unchanged in all these three conditions. Phosphorylase (EC 2.4.1.1) activity was not affected in cortisone-treated rats but was depressed in diabetic and growth hormone-treated rats.

Alanine Transaminase↗