Search PubMed⌕ Search

Biomedical subjects

S V Chandra

Publications and source records attributed to S V Chandra.

At least 91 records · Page 5Linked to original sources
PubMed1981

Striatal dopamine turnover and L-dopa treatment after short-term exposure of rats to manganese.

The turnover rate of striatal dopamine (DA) and the effect of L-dopa treatment was investigated in rats after the daily oral administration of MnCl2 . 4H20 for a period of 30 days. The turnover rate of striatal DA, as determined by the administration of alpha-methyl-p-tyrosine, increased significantly in manganese-exposed rats. L-Dopa administration resulted in a significant elevation in the levels of DA and its metabolite, homovanillic acid, in manganese-exposed rats, but these neurochemical changes could not be correlated with the concentration of manganese in the striatum. We therefore advise the L-dopa therapy should not be tried in early manganese intoxication, as it may aggravate manic symptoms due to marked increase in brain DA.

Animals↗
PubMed1981

Effect of manganese and copper interaction on behavior and biogenic amines in rats fed a 10% casein diet.

Manganese chloride (1 mg manganese/ml drinking water) and copper sulphate (250 mg copper/kg diet) were administered daily for 30 days to growing rats maintained on a 10% casein diet. Manganese in combination with copper produced impairment in the learning ability and memory of rats in either dietary group, with greater alterations in those receiving a 10% casein diet. Hyperactivation due to the combined effects of the metal ions was identical in both dietary groups. The behavioral aberrations were associated with a marked accumulation of Cu in the brain of rats receiving the 10% casein diet. Combined exposure of Mn and Cu also produced a greater elevation in the levels of dopamine (DA) and norepinephrine (NE) and a depression of 5-hydroxytryptamine (5-HT) in the brain of animals fed with a 10% casein diet compared to the animals receiving the 21% casein diet. Thus the animals receiving the 10% casein diet appear to be more vulnerable to the neurotoxic effects of a combined exposure to manganese and copper. However rats maintained on the 21% casein diet and receiving both manganese and copper showed almost identical changes to those observed after manganese administration alone.

Animals↗
PubMed1981

Serum ceruloplasmin in manganese-treated rats.

Rats were exposed to manganese (Mn) (6 mg/kg) daily for 30 days. The content of ceruloplasmin decreased significantly by 19.5% while copper (Cu) content was reduced by 27.8% in the serum of Mn-treated animals. These alterations were associated with a marked increase in the Cu content of liver and brain. The significant decrease in serum Cu and ceruloplasmin may serve as useful parameters for early diagnosis of Mn poisoning.

Animals↗
PubMed1981

Toxicity of endosulfan and manganese chloride: cumulative toxicity rating.

There has been, in general, no accepted comparable way to express the effects of repeated doses. This study was designed to provide information on cumulative toxicity of manganese chloride (MnCl2), endosulfan, and a mixture of these compounds and to suggest cumulative toxicity rating. Male mice were given the test compound i.p. 6 days/week for a minimum for 10 weeks and until the cumulative LD50 remained constant for 3 consecutive weeks. Using a ratio between a single dose and weekly cumulative LD50 (CLD50), cumulative toxic factors (CTF) were determined. The CTF for weeks 1-13 for MnCl2 ranged from 0 to 3.48; endosulfan LD50 and CLD50 values for a mixture of MnCl2 and endosulfan were higher than the expected values, indicating a greatly reduced toxicity of a mixture, when given either in a single dose or repeated doses. Using the CLD50 criterion as laid down in this study, the cumulative toxicity rating, class 1 to 6, has been suggested so as to have a comparative assessment of th cumulative potential of several compounds.

Animals↗
PubMed1981

Concentrations of striatal catecholamines in rats given manganese chloride through drinking water.

Male albino rats were exposed to manganese through drinking solution containing MnCl2 . 4H2O (1 mg/ml) in water. The contents of catecholamines, homovanillic acid, manganese and the activity of monoamine oxidase (MAO) were measured in the corpus striatum at different time intervals up to a period of 360 days. The contents of tyrosine in the corpus striatum and serum were also estimated. Manganese treatment produced an initial increase in the contents of dopamine (DA), norepinephrine (NE), homovanillic acid (HVA) and tyrosine in the corpus striatum. This was followed by a period when concentrations were almost normal (dopamine from 120 to 240 days, norepinephrine at 180 and 240 days and homovanillic acid at 240 days after manganese administration). Thereafter the contents of these substrates declined significantly at 300 and 360 days of treatment. However, these alterations were not correlated with the concentrations of manganese in this region, which gradually increased up to 240 days, and thereafter remained constant until the termination of the experiment. The underlying biochemical mechanisms of manganese-induced sequential changes in the striatal contents of catecholamines have been discussed in relation to the development of psychiatric and neurological phases of manganese poisoning.

Animals↗
PubMed1981

Manganese toxicity: lipid peroxidation in rat brain.

Albino rats were given intraperitoneally manganese chloride (Mn2+, 4mg/kg) daily for a period of 30 days. Manganese significantly inhibited the lipid peroxidation potential of treated rat brain without altering the contents of iron and ascorbic acid, the two prooxidant factors. In vitro lipid peroxidation studies in the fresh and heated brain homogenates showed almost a non-enzymatic mechanism of inhibition by this metal ion. 30 micrometers Mn2+ concentrations completely inhibited the formation of malonaldehyde (MDA) at 3 hours of incubation. Iron was found to reverse, to some extent, the effect of manganese on in vitro lipid peroxide formation in the mitochondrial fraction of brain and at concentrations of 5 micrometers Fe2+ the amount of MDA formed is comparable to that observed with 1 micro meter Fe2+ in the mitochondrial fraction without manganese. These observations suggest that the central nervous system toxicity of manganese may not be associated with accelerated in vivo lipid peroxidation. However, the mechanism of iron induced reversal on in vitro inhibition of lipid peroxidation by manganese is not understood, at present.

Animals↗
PubMed1981

Effect of manganese on synthesis of brain catecholamines in growing rats.

The effect of short-term exposure of manganese on the synthesis of brain catecholamines in growing rats has been investigated by using two methods, 1) measuring the amount of conversion of 3,5-3H-tyrosine to 3H-labelled dopamine and norepinephrine, and 2) measuring the rate of decline of endogenous dopamine and norepinephrine following inhibition of their synthesis with alpha-methyl-p-tyrosine. The magnitude of conversion of 3,5-3H-tyrosine to 3H-dopamine and 3H-norepinephrine in the brain at 60 min after the administration of labelled amino acid to the manganese treated rats (1 mg MnCl2.4H2O/ml of water for 30 days) was significantly greater than observed in control rats. Manganese also increased turnover of dopamine and norepinephrine to a greater extent in the brains of treated animals.

Animals↗
PubMed1981

An exploratory study of manganese exposure to welders.

Sixty welders (20 each from Plants A, B, and C) and 20 control subjects were investigated for the possible occurrence of manganese poisoning among welders exposed to the welding fumes containing this metal. Ten, 9, and 5 welders from Plants B, C, and A, respectively, were diagnosed as suspected cases of early manganese poisoning. The diagnosis was based on the proof of overexposure to manganese by the findings of increased urinary levels of this metal, signs of early neurological involvement, and increased contents of serum calcium. These results are discussed in relation to the manganese concentration in the air around the welder's breathing zones.

Adult↗
PubMed1980

Managanese-induced biochemical changes in growing versus adult rats.

Manganese chloride was administered daily intraperitoneally to growing and adult rats for a period of 30 days to compare certain biochemical parameters in both groups of animals. Marked alterations in the levels of dopamine and norepinephrine in the brain was observed in manganese-treated growing rats. Furthermore, the contents of tyrosine, tryptophan in blood, liver, and brain have been significantly altered in these animals. Identical manganese administration to adult rats had no effect on the contents of tyrosine in liver and brain, nor tryptophan, and dopamine in the brain. Some of the parameters which were altered in the adult rats were less in magnitude compared to the growing animals. The experiments indicated higher susceptibility of the growing rats to the toxic effects of this metal.

Aging↗
PubMed1980

Combined effect of metals on biogenic amines and their distribution in the brain of mice.

The toxic effects of manganese in combination with iron or copper on the brain tissue of mice were investigated. The combined administration of manganese and iron decreased the accumulation of manganese in the brain compared to manganese treatment alone. This indicated that excess iron may influence the absorption of manganese. Combined exposure to manganese and copper resulted in marked accumulation of copper in the brain. This is of great concern, since excess copper in brain produces incoordination in body movements. Thus, the combined exposure of these two metals, even in permissible limits, may produce serious brain dysfunctions. The combined administration of manganese with iron or copper has also significantly altered the levels of brain tryptophan and 5-hydroxytryptamine.

Animals↗
PubMed1980

The effect of manganese administration, alone or combined with zinc, mercury and cadmium, on the tissue levels of these elements in rats.

Manganese chloride was administered alone or in combination with zinc chloride, mercuric chloride and cadmium chloride i.p. to rats for 30 days to investigate the effect of interaction of these elements on their content in brain, liver and kidney. Significant changes in the accumulation of these metals after combined exposure indicated that metabolic interactions occur. Alterations in the tissue contents of manganese, zinc, mercury and cadmium after combined administration may reflect changes at the absorptive sites or in excretory pattern.

Animals↗
PubMed1980

Neuromelanin in manganese-exposed primates.

Monkeys developed muscular weakness and rigidity of the lower limbs after 18 months exposure to manganese. These are neurological signs typical of chronic manganese intoxication. Marked neuronal degeneration with depigmentation was noticed in the region of substantia nigra. Significance of depigmentation in relation to the depletion in the contents of brain dopamine in chronic manganese intoxication has been discussed.

Animals↗
PubMed1980

Manganese induced testicular changes in monkeys.

Oral administration of manganese chloride (25 mg/kg b. w. daily) to monkeys for a period of 18 months produced congestion and marked increase in weight of testis. Histopathologic examination revealed interstitial oedema and degeneration of seminiferous tubules. Activities of succinic dehydrogenase, glucose-6-phosphate dehydrogenase and acid phosphatase were significantly inhibited whereas NADH-diaphorase and alkaline phosphatase activities showed only slight inhibition in seminiferous tubules of treated monkeys. It was concluded that chronic exposure to manganese does not produce sever degenerative changes in the testis earlier than metal induced encephalopathy in primates.

Acid Phosphatase↗
PubMed1979

The interaction between ethanol and manganese in rat brain.

The effect of combined administration of ethanol and manganese on the brain tissue of rats was investigated to evaluate the role of alcohol ingestion in inducing susceptibility to manganese poisoning. Ethanol and manganese alone and the combination of the two were administered orally daily to the rats for 30 days. Almost identical increase in the brain contents of manganese in rats receiving the metal alone and in combination with ethanol indicates that ethanol administration does not influence the accumulation of manganese in that organ. The copper contents of brain also increased to almost the same extent in these two groups. Synergistic effect of ethanol and manganese was noticed on increasing the activity of ATPase and RNase while marked antagonistic effect was observed on the activity of MAO. The mechanism and the significance of these neurochemical alterations occurring after the administration of ethanol and manganese have been discussed.

Animals↗
PubMed1979

Effect of di-(2-ethylhexyl) phthalate on rat liver injured by chronic carbon tetrachloride treatment.

The effect of Di-(2-ethylhexyl) phthalate (DEPH), a widely used plasticizer, was studied using histopathological and biochemical parameters on rat liver injured by carbon tetrachloride (CCl4). The mild centrilobular necrosis observed with CCl4 (7.7 mmol/kg subcutaneously and biweekly up to 38 days) and mild congestion and bile duct proliferation produced by DEHP (2.5 mmol/kg intraperitoneally daily for ten days after the day 28 of experiment) were modified into extensive necrosis of the parenchymal cells when the animals received both chemicals. Groups of hepatocytes mostly at the periphery of the lobules also showed coagulative necrosis and some central and portal veins were completely occluded. Alterations in the activity of serum and liver enzymes of the animals receiving both chemicals were not significantly different from those treated with CCl4 alone, except in case of glucose-6-phosphatase (G-6Pase) and SGPT. The characteristic decrease of G-6-Pase and increase of SGPT was less marked. Although the exact mechanism of the chemical interaction between CCl4 and DEHP is not known, the results indicate their combined toxic potentiality.

Adenosine Triphosphatases↗