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Biomedical subjects

S V Chandra

Publications and source records attributed to S V Chandra.

At least 109 records · Page 6Linked to original sources
PubMed1978

The interaction between manganese and ethanol in rats.

The effects of manganese and ethanol interaction on some chemical constituents of the liver and serum of rats were investigated in order to assess the influence of these substances in inducing susceptibility to manganese poisoning. Manganese and ethanol alone or in combination were administered to the rats as drinking solutions for a period of 30 days. Both the chemicals had a synergistic effect in altering the activity of SDH and ATPase in the liver of rats. The combined treatment also produced significant increase in the activity of adenosine deaminase and alpha-amylase in the liver and serum respectively. Furthermore, the accumulation of manganese in the liver and the increase in the calcium content of the serum were significantly greater after combined ethanol and manganese administration--than either of them alone. These alterations indicate that the toxic effects of manganese are enhanced when the metal and ethanol interact in the biological system.

Adenosine Deaminase↗
PubMed1978

Comparative toxicity of trivalent and hexavalent chromium to rabbits. III. Biochemical and histological changes in testicular tissue.

The administration of trivalent and hexavalent chromium compounds produced inhibition of the activity of succinic dehydrogenase, adenosine triphosphatase and acid phosphattase accompanied by cellular degeneration with complete absence of spermatocytes in the testis of rabbits. The biochemical and histological changes were more marked in the animals treated with the trivalent chromium than those exposed to hexavalent chromium and were progressive with the duration of exposure.

Acid Phosphatase↗
PubMed1977

Levels of sulfhydryls and sulfhydryl-containing enzymes in brain, liver and testis of manganese treated rats.

The effect of manganese on sulfhydryls and sulfhydryl-containing enzymes in brain, liver and testis of rats was investigated. Manganese produced lowering in the contents of non-protein sulfhydryl groups and inhibited the activity of glucose-6-phosphate dehydrogenase and glutathione reductase in these tissues. The contents of the metal increased significantly in brain, liver and testis of manganese administered rats. The significance of these findings is discussed.

Animals↗
PubMed1977

Biochemical and morphological changes in some organs of rats in nickel intoxication.

Biochemical and histological alterations in liver, kidney, testis and myocardium of albino rats were investigated at various intervals after daily administration of nickel sulphate. No significant changes were observed during the initial periods of the treatment, but longer exposures produced marked enzymatic and histopathological alterations in all the four organs examined. The severity of the histological lesions was found to be directly related to the duration of the treatment.

Animals↗
PubMed1977

Comparative toxicity of trivalent and hexavalent chromium to rabbits. II. Morphological changes in some organs.

Toxicity of trivalent and hexavalent chromium compounds was investigated in experimental rabbits to ascertain health hazards among industrial workers of miners occupationally exposed to such chemicals. Brain, kidney and myocardium showed a tendency to accumulate chromium irrespective of its valency state; the morphological changes were more marked in animals exposed to hexavalent chromium. However, no definite co-relation could be observed between the concentration of the metal and the degree of histological changes in these organs.

Animals↗
PubMed1977

Effect of manganese on neonatal rat: manganese concentration and enzymatic alterations in brain.

Suckling rats were exposed for 15 and 30 days to manganese through the milk of nursing dams receiving 15 mg MnCl2--4H2O/kg/day orally and after which the neurological manifestations of metal poisoning were studied. No significant differences in the growth rate, developmental landmarks and walking movements were observed between the control and manganese-exposed pups. The metal concentration was significantly increased in the brain of manganese-fed pups at 15 days and exhibited a further three-fold increase over the control, at 30 days. The accumulation of the metal in the brain of manganese-exposed nursing dams was comparatively much less. A significant decrease in succinic dehydrogenase, adenosine triphosphatase, adenosine triphosphatase, adenosine deaminase, acetylcholine esterase and an increase in monoamine oxidase activity was observed in the brain of experimental pups and dams. The results suggest that the developing brain may also be susceptible to manganese.

Acetylcholinesterase↗
PubMed1976

Role of iron deficiency in inducing susceptibility to manganese toxicity.

Daily intraperitoneal administration of manganese chloride (15 mg/kg) to rats, maintained on an irondeficient diet, produced marked alterations in the activity of succinic dehydrogenase, monoamine oxidase, and in the morphology of the liver. Manganese accumulation was also significantly increased in such rats than after similar treatment to normally fed rats. Iron deficiency leads to increased absorption of manganese which is responsible for increased susceptibility to manganese toxicity in these animals.

Animals↗
PubMed1976

Effect of manganese on the levels of DNA, RNA, DNase and RNase in cerebrum, cerebellum and rest of brain regions of rat.

Levles of DNA, RNA, DNase, RNase and manganese in different regions of rat brain were studied after daily administration of manganese chloride (8 mg MnCl2-4H2O/kg intraperitoneally) for a period of 120 days. DNA and RNA contents decreased significantly in cerebrum, cerebellum and rest of the brain regions after manganese treatment. A decrease in the DNase and an increase in the RNase activity was observed in the cerebellum and rest of brain region of the manganese treated animals. The manganese content increased significantly in all the regions of the brain, the maximum concentration being in the rest of brain portion. The presence of excess manganese in brain presumably leads to alterations in the functional activity of lysosomal enzymes. The decrease in the levels of nucleic acids is perhaps a consequence of the degenerating and dead neurones.

Animals↗
PubMed1975

Chelation in metal intoxication II: In vitro and in vivo effect of some compounds on brain, liver, and testis of rats treated with manganese sulphate.

Some structurally different compounds were examined for their ability to remove manganese as their chelates from brain, liver and testis and the sub-cellular fractions of brain and liver of manganese administered rats. An attempt was also made to corelate the removal of the metal with the recovery of altered activity of succinic dehydrogenase in these organs. While all the compounds were able to remove the metal significantly from in vivo brain, liver and testis, they could fully restore the enzyme activity only in brain. However, there was no significant improvement in the altered morphology of the tissues in eight days of treatment with the chelating agents.

Animals↗