Biomedical subjects

M N Subhash

Publications and source records attributed to M N Subhash.

14 recordsLinked to original sources

PubMed1992

CSF amine metabolites in depression.

The amine metabolites, namely homovanillic acid (HVA) and 5-hydroxy indoleacetic acid (5-HIAA) were measured in cerebrospinal fluid (CSF) of depressives (n = 30) and controls (n = 30). Depressed patients had significantly lower HVA levels than controls. No significant differences were noted between the two groups in 5-HIAA levels. However, the differences between the groups for the CSF HVA/5-HIAA ratio were larger than those for the CSF HVA alone (p less than 0.01 versus p less than 0.025, respectively). HVA levels correlated positively with monoamine oxidase activity and adenosine deaminase activity.

Adult↗

PubMed1992

Erythrocyte membrane sodium-potassium adenosine triphosphatase activity in affective disorders.

Erythrocyte membrane Na+,K(+)-ATPase activity was studied in drug naive patients with bipolar (BP) mania (n = 62) and unipolar (UP) depression (n = 60) and normal controls (n = 66). Compared to controls there was a significantly decreased Na+,K(+)-ATPase activity in UP depressives but no change in BP manics. However, lithium treatment caused a significant increase in Na+,K(+)-ATPase activity although there was no correlation between plasma lithium levels and enzyme activity. Plasma cortisol correlated inversely with Na+,K(+)-ATPase in UP depressives. Interestingly, the lithium responders [less than 50% Beck Rafaelson's Mania Rating Scale (BRMS) score] showed a significant increase in Na+,K(+)-ATPase activity compared to lithium nonresponders (greater than 50% BRMS score). These observations indicate that monitoring of Na+,K(+)-ATPase activity during lithium therapy is useful to predict a therapeutic response.

Adult↗

PubMed1991

Role of glutathione reductase system in disulfiram conversion to diethyldithiocarbamate.

Experiments were carried out to establish the role of glutathione reductase (GR), if any, in the metabolic conversion of disulfiram (DS) to diethyldithiocarbamate (DDC). It was observed that, under standard assay conditions, whereas DS was incorporated as a substrate instead of oxidised glutathione (GSSG), the enzymes from both human liver extract and yeast sources failed to reduce the parent compound, implying that glutathione reductase perse do not reduce disulfiram. However, the incorporation of disulfiram into an assay system comprising of GSSG, NADPH and reductase resulted in DS reduction to DDC. Further, the observation, that the GR assay system devoid of either GSSG or NADPH was found to lack DS reducing ability, implies that GSH as a reaction product of GR system is responsible for the reduction of DS to DDC. The results of in-vitro experiments indicated that GSH perse could reduce DS to DDC nonenzymatically, with a stoichiometric relationship of 2:1. Thus it is inferred that GR perse do not reduce DS, whereas GSH, as an intermediary metabolite of GR system, brings about non-enzymatic reduction of DS via a sulfhydral group exchange reaction.

Disulfiram↗

PubMed1991

Effect of manganese on biogenic amine metabolism in regions of the rat brain.

The effect of prolonged exposure to low-level manganese (Mn) on regional levels of biogenic amines in the rat brain was studied. Rats were given Mn in drinking-water for 90 days, which resulted in a two- to three-fold accumulation of Mn in all regions of the brain. After exposure, dopamine beta-hydroxylase (DBH), monoamine oxidase (MAO), dopamine (DA) and serotonin (5-HT) were measured in regions of the brain. There was a significant inhibition of DBH in the striatum (P less than 0.01), hypothalamus (P less than 0.01), mid-brain (P less than 0.001) and cortex (P less than 0.01). MAO was also decreased significantly in the cerebellum and cortex (both P less than 0.01). The striatum showed a decrease in DA content, but this was not significant. However, the hippocampus showed a significant decrease (P less than 0.01) and the mid-brain showed a significant increase (P less than 0.01) in DA levels. No significant changes were observed in 5-HT levels in any region, except for an increase in the cortex (P less than 0.01). It was observed that prolonged exposure of rats to low-level Mn affects both DBH and MAO, and that this effect is region-specific. However, the effect of Mn on biogenic amines seems to be variable, and this might explain the variable signs and symptoms observed in the various phases of Mn toxicity in humans.

Administration, Oral↗

PubMed1990

Regional distribution of dopamine beta-hydroxylase and monoamine oxidase in the brains of rats exposed to manganese.

The regional distribution of dopamine beta-hydroxylase (DBH) and monoamine oxidase (MAO) in rat brain was compared in control rats and rats given manganese in drinking-water (1 mg Mn/ml) for 30 days. In treated rats there was a significant accumulation of Mn in almost all regions of the brain except the hippocampus. Accumulation was highest in the hypothalamus, cortex and striatum. After Mn exposure, DBH activity was significantly decreased (in comparison with the controls) in the hypothalamus, striatum, mid-brain, cerebellum and cortex. A significant increase in MAO activity was found in the striatum, hypothalamus, mid-brain, hippocampus and medulla. The effects of Mn on these enzymes suggests the involvement of biogenic amines like dopamine, norepinephrine and serotonin during Mn toxicity. The effect of Mn is region specific and in certain regions the action of Mn on DBH differs from that on MAO. These different effects of Mn on DBH and MAO in different regions of the brain might explain the variable symptoms seen in Mn-induced neurotoxicity in humans.

Administration, Oral↗

PubMed1989