Search PubMed⌕ Search

Biomedical subjects

Y Singh

Publications and source records attributed to Y Singh.

At least 109 records · Page 6Linked to original sources
PubMed1988

Pulmonary and hepatic glutathione levels, glutathione shuttle enzymes and lipid peroxidation in rats exposed intratracheally to coal fly ash.

Fly ash and fly ash residue increased the formation of conjugated dienes and the levels of oxidized glutathione (GSSG) and reduced the levels of reduced glutathione (GSH) in lung and liver whereas fly ash extract administration had no effect on the formation of conjugated dienes and glutathione levels in lung and liver. Fly ash and fly ash residue reduced the activity of glutathione reductase both in lung and liver but did not alter the activity of glutathione peroxidase. Fly ash and fly ash extract significantly increased glucose-6-phosphate dehydrogenase activity in lung whereas in liver, fly ash and fly ash residue reduced the activity of glucose-6-phosphate dehydrogenase. Fly ash residue did not alter the activity of glucose-6-phosphate dehydrogenase in lung whereas fly ash extract was not effective in liver.

Animals↗
PubMed1987

Daunomycin inhibits the uptake of adenine, amino acids, and glucose into cardiac myocytes.

Daunomycin and adriamycin are widely used antitumor agents which induce dose-dependent cardiotoxicity. The mechanisms by which daunomycin causes cardiotoxicity have been investigated in neonatal rat cardiac myocytes maintained in tissue culture. Daunomycin inhibited the uptake of adenine, amino acids, and deoxyglucose in a dose-dependent fashion. The uptake of both adenine and methionine was inhibited without any delay while the glucose uptake (deoxyglucose) was inhibited after a delay of 2 hr. Since daunomycin affected the uptake of both adenine and amino acids without any delay and since daunomycin did not affect the incorporation of adenine into nucleotide and amino acids into proteins once these were transported into the cell, it is possible the daunomycin exerted these effects by acting directly on the cell membrane. Thus, one of the early toxic manifestations of anthracycline antibiotics may be on the transport of nutrients such as amino acids, glucose, and adenine.

Adenine↗
PubMed1987

Induction of hepatic drug metabolizing enzymes by coal fly ash in rats.

The effect of intratracheal administration of fly ash, its benzene-extracted residue and the benzene extract has been studied on the activities of hepatic mixed-function oxidases in the rat. Fly ash and its fractions significantly increased the levels of cytochrome P-450, cytochrome b5, cytochrome b5 reductase, NADPH-cytochrome c reductase, aminopyrine N-demethylase, aniline hydroxylase, and glutathione S-transferase in a dose-dependent manner. Phenobarbital or 3-methylcholanthrene treatment along with the administration of fly ash or its fractions showed an additive effect on the activities of the mixed-function oxidases. The observed effects were due to chemical component, i.e., organic and inorganic fractions of fly ash, and not due to its particulate nature. This was shown by the administration of glass beads which did not cause any alteration in the activities of hepatic mixed-function oxidases.

Aminopyrine N-Demethylase↗
PubMed1987

Valproic acid-induced increase in carnitine acetyltransferase in rat hepatocytes is not due to an induction of peroxisomes.

Valproic acid induced a dose-dependent increase in carnitine acetyltransferase (CAT) activity in rat hepatic mitochondrial fractions isolated by differential centrifugation. An increase in CAT and carnitine palmitoyltransferase (CPT) also occurred in cultured rat hepatocytes in a concentration-and time-dependent fashion. A maximal increase of 8-fold in the activity of CAT and 2-fold in the activity of CPT was induced by 3 mM valproic acid in 72 h. Valproic acid had no effect on cytochrome P-450 levels in cultured rat hepatocytes. Electron-microscopic examination of rat hepatocytes showed that there was no increase in the number of peroxisomes but there was a marked proliferation of mitochondria in parallel with an increase in glutathione level and succinic dehydrogenase in the liver cells after incubation with valproic acid in vitro.

Acetyltransferases↗
PubMed1986

Formation of superoxide and hydroxyl radicals from 1-methyl-4-phenylpyridinium ion (MPP+): reductive activation by NADPH cytochrome P-450 reductase.

Formation of free radical intermediates from 1--methyl-4-phenylpyridinium ion(MPP+) has been studied using spin-trapping techniques. Incubation of MPP+ with purified NADPH cytochrome P-450 reductase and NADPH under anaerobic conditions failed to produce any detectable radical intermediates. However, in the presence of air and a spin-trap, a significant stimulation of superoxide and hydroxyl radicals was detected. Formation of these toxic radicals from MPP+ was inhibited by superoxide dismutase, catalase, and ethanol. Under identical conditions, however, considerably less of these radicals were formed with MPP+ in comparison to paraquat, a lung toxin containing two pyridinium moieties.

1-Methyl-4-phenylpyridinium↗
PubMed1986

Inhibition of overall protein and RNA synthesis as a mechanism for the tunicamycin induced decrease in cytochrome P-450 in rat hepatocytes.

In rat hepatocytes maintained in culture, cytochrome P-450 and NADPH cytochrome c reductase activities were decreased by tunicamycin in a dose and time dependent fashion. The effect of tunicamycin was mainly due to inhibition of protein synthesis. Tunicamycin decreased L-[35S] methionine incorporation into many proteins, including a 52 kDa cytochrome P-450 isozyme. Tunicamycin also reduced RNA synthesis. These results indicate that tunicamycin decreased cytochrome P-450 levels in hepatocytes by inhibiting protein and RNA synthesis.

Animals↗
PubMed1985

Inhibition of protein synthesis: a basis for tunicamycin-induced decrease in rat liver cytochrome P-450.

Tunicamycin caused a dose and time dependent decrease in cytochrome P-450 in rat liver. A dose of 50 micrograms/kg caused a decrease of about 50% in 72 hours. A similar decrease in the activities of rat liver microsomal aniline hydroxylase, aminopyrine N-demethylase and ethoxycoumarin O-deethylase were also seen after the tunicamycin treatment. Tunicamycin also suppressed food and water intake but the decrease in cytochrome P-450 was not related to these effects. NADPH cytochrome c reductase was not markedly decreased by tunicamycin. A decrease in cytochrome P-450 was also observed in cultured rat hepatocytes treated with tunicamycin. It decreased incorporation of [35S]-methionine into total proteins as well as into various cytochrome P-450 isozymes of rat hepatocytes. This indicates that a decrease in protein synthesis may be responsible for the tunicamycin-induced decrease in cytochrome P-450 and drug metabolism.

Animals↗
PubMed1984

Inhibition of hepatic phosphatidylcholine synthesis by malathion in rats.

Rats maintained on a 20% casein diet were given malathion orally throughout the feeding period (100 mg/kg body weight/day, dissolved in groundnut oil). Hepatic choline kinase (EC 2.7.1.32) and cholinephosphate cytidyltransferase (EC 2.7.7.15) activities were inhibited, whereas cholinephosphotransferase (EC 2.7.8.2) activity was not affected by malathion administration. Incorporation of [methyl-14C]L-methionine into hepatic microsomal phosphatidylcholine was significantly reduced by malathion administration.

Animals↗
PubMed1983

Teaching TMR children to read using integrated picture cueing.

A rebus program was compared with a new picture-cue method for teaching TMR children to read. Two groups of 20 TMR children each participated in a 26-week course during which recognition and transfer to standard orthography were measured. The cued-word group was significantly superior in reading words in standard orthography both during training (75 percent compared with 25 percent transfer) as well as at the end of training (96 vs. 50 percent transfer). The results justify further exploration of the picture-cueing method both for retarded and for beginning readers in general.

Adolescent↗