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Biomedical subjects

S V Chandra

Publications and source records attributed to S V Chandra.

At least 73 records · Page 4Linked to original sources
PubMed1984

Concurrent exposure of lead and manganese to iron-deficient rats: effect on lipid peroxidation and contents of some metals in the brain.

Iron-deficient rats were co-exposed to manganese and lead to study lipid peroxide formation and contents of lead, manganese, copper, iron, zinc and calcium in the brain. Concurrent exposure to lead and manganese increased the lipid peroxidation potential of brain in iron-deficient rats. The concentration of lead, manganese and copper in the brain of iron-deficient rats increased to a greater magnitude after concurrent exposure to manganese and lead, compared with that observed after the exposure of either of the metals alone. Since copper is a potent inhibitor of transport ATPase in the brain, its significant increase, coupled with increased lipid peroxidation in the brain of iron-deficient rats, may be responsible for enhanced susceptibility of iron-deficient rats to the neurotoxic effects after the combined exposure to lead and manganese.

Animals↗
PubMed1984

Effect of interaction of heavy metals on (Na+ -K+) ATPase and the uptake of 3H-DA and 3H-NA in rat brain synaptosomes.

The effect of interaction of Mn2+, Pb2+ and Cd2+ on (Na+ -K+) ATPase and uptake of labelled dopamine (3H-DA) and labelled noradrenaline (3H-NA) were studied in vitro in rat brain synaptosomes. The inhibition of (Na+ -K+) ATPase by Pb2+ and Cd2+ alone was concentration dependent, however, Mn2+ had almost no effect on the activity of this enzyme. Interaction of Cd2+ with either Pb2+ or Mn2+ was most powerful in inhibiting the activity of synaptosomal transport ATPase. Lower concentrations of Pb2+ increased while higher concentrations inhibited synaptosomal uptake of 3H-DA and 3H-NA. Lower concentrations of Cd2+ increased the uptake of 3H-DA while at concentrations of 100 microM, the uptake was inhibited, this metal had strong inhibitory effect on the uptake of 3H-NA. Mn2+ had inhibited the uptake of labelled amines. Interaction of Mn2+ with Pb2+ or Cd2+ produced inhibition on the uptake of 3H-DA and 3H-NA. The results of the uptake of biogenic amines in the presence of metal ions apparently had no correlation with the activity of (Na+ -K+) ATPase which is involved in the active transport of cations across cell membranes.

Animals↗
PubMed1984

Nature of 54Mn binding protein in rat brain, liver and serum.

Studies were undertaken to investigate the 54Mn binding protein in rat serum, liver and brain. Equilibrium dialysis pattern in three biological media with 54Mn against distilled water showed a rectangular hyperbola after 24 hr dialysis. 54Mn in the bag was in the non-dialysable form, presumably bound to protein. Gel filtration studies with 54Mn bound protein showed that 54Mn had a specific carrier protein, which was identical for all the three biological media tested. The electrophorogram of concentrated 54Mn protein with Comassie blue stain for protein and PAS stain for glycoprotein showed a single band with an equal RF value clearly indicating the glycoprotein nature of 54Mn binding protein. Sulphydryl groups were absent and it had molecular weight of 6.3 X 10(4) dalton.

Animals↗
PubMed1984

Neurotransmitters and neurotransmitter receptors in developing and adult rats during manganese poisoning.

Manganese neurotoxicity has been recognized among industrial workers as a consequence of chronic exposure to the metal in the form of fumes or dust. Hazards for the general population, including newborn and developing children, and other living organisms may also originate from prolonged low-level exposure to manganese and its organometallic compounds released into the environment as a result of their variety of applications. Experimental evidence has been presented to show that developing mice and rats are not able to excrete manganese for first 17-18 days of life, with excessive tissue accumulation, and their brain is more susceptible to the neurotoxic effects of manganese. Prolonged exposure to manganese causes depletion of dopamine and other monoamines in adult rats. The short-term exposure produces an increase in the binding of dopaminergic antagonist [3H]-spiroperidol to striatal membranes without affecting the other neurotransmitter receptors at low doses (10 mg/kg X 15). A higher dose (15 mg/kg X 15), causes a decrease in cerebral GABA, frontal cortical serotonin and striatal muscarinic binding and an increase in binding of [3H]-spiroperidol to striatal membranes. No significant changes occur in the levels of dopamine or serotonin at either of these two doses. The neonatal rat in certain respects shows a different effect on dopamine levels and receptor sensitivity. Exposure to manganese causes an increase in levels of dopamine and norepinephrine. Neonatal exposure to manganese (10 mg/kg X 15) produces a decrease in binding of [3H]-spiroperidol to striatal membranes and of serotonin to frontal cortical membranes.

Aging↗
PubMed1983

Effects of manganese on rat brain microsomal Mg2+-Na+-K+-ATPase: in vivo and in vitro studies.

The effect of manganese on brain microsomal Mg2+-Na+K+-ATPase was examined both in vitro and in vivo. Daily intraperitoneal administration of MnCl2 . 4H2O (Mn2+, 6 mg/kg) to the rats for a period of 90 days produced 10% (P less than 0.05) inhibition in the activity of Mg2+-ATPase, and 72 and 63% increases in the contents of manganese and copper, respectively, in the microsomal fraction of brain. In in vitro studies, lower concentrations of Mn2+ activated while higher concentrations inhibited the activity of brain microsomal ATPase. Addition of equal concentrations of Mn2+ + Cu2+ (8 mM) in vitro produced 8% inhibition in the activity of Mg2+-ATPase and 83% inhibition in Na+-K+-ATPase. Free Cu2+ ions were able to antagonize the effect of Mn2+ on ATPase in vitro and inhibited the activity of Mg2+-Na+-K+-ATPase with more pronounced effect of Na+-K+-ATPase. The lack of change in the activity of Na+-K+-ATPase in the brain microsomes of rats administered manganese, in spite of a significant increase in copper, could not be explained. It is, however, evident that a manganese-induced elevation in brain copper was not responsible for initiating biochemical changes in manganese neurotoxicity.

Animals↗
PubMed1983

Psychiatric illness due to manganese poisoning.

Rats were exposed to manganese (1 mg/ml through drinking water) daily to study behavioral and neurochemical changes 14 and 30 days after the treatment. Manganese produced hyperactivation after 14 and 30 days with greater magnitude of alteration at the latter period. Reduction in the percentage of conditional avoidance response and increase in fighting score were also observed after 30 days. These behavioral changes were associated with increased levels of striatal dopamine and norepinephrine in rats exposed to manganese. Thus, it was indicated that increased turnover of striatal catecholamines was responsible for producing behavioral changes in early manganese intoxication.

Animals↗
PubMed1983

Effects of certain mono-, di- and trivalent metal cations on the K+-stimulated p-Nitrophenyl phosphatase in rat brain.

The effects of certain monovalent (Ag+1 and Li+1), divalent (Hg+2, Cu+2, Zn+2, Co+2, Fe+2, Pb+2, Mn+2, Sn+2, Ni+2, and Se+2) and trivalent (Fe+3, As+3, and Al+3) metals on a mitochondrial preparation of K+-stimulated-p-nitrophenyl phosphatase (K+-PNPPase) from rat brain were studied. Except for salts of Ni+2, Se+2 and Li+1, which irrespective of concentration failed to produce 50% inhibition, all of the metals examined were found to be potent inhibitors of the enzyme with 150 values of 0.24 microM for Ag+1 among the monovalent, 0.70, 30, 37, 38, 47, 60, 62, 490 and 850 microM for Hg+2, Cu+2, Cd+2, Zn+2, Co+2, Fe+2, Pb+2, Mn+2 and Sn+2, respectively, among the divalents and 100, 550 and 870 microM for Fe+3, As+3, and AL+3 respectively, among the trivalents. Salts of silver and mercury were the most toxic for this enzyme. All metals showed concentration dependent inhibition except lithium. The order of their potency was Ag+1 greater than Hg+2 greater than Cu+2 greater than Cd+2 greater than Zn+2 greater than Co+2 greater than Fe+2 greater than Pb+2 greater than Fe+3 greater than Mn+2 greater than As+3 greater than Sn+2 greater than Al+3 greater than Ni+2 greater than Se+2 greater than Li+1.

4-Nitrophenylphosphatase↗
PubMed1982

Hepatic effects of orally administered styrene in rats.

Adult male rats receiving styrene by gavage (200 or 400 mg kg-1, 6 days a week) for 100 days exhibited a significant dose-dependent increase in hepatic benzo[a]pyrene hydroxylase and aminopyrine-N-demethylase, a decrease in glutathione-S-transferase and no change in glucose-6-phosphatase. A decrease in the activity of mitochondrial succinic dehydrogenase and beta-glucuronidase was also observed. Activity of acid phosphatase was decreased only at the higher dose level. Levels of serum glutamic oxaloacetic transaminase and glutamic pyruvic transaminase were elevated only at the higher dose level. The absolute and relative weights of the liver of control and treated animals showed no significant difference. Histopathological studies of the liver tissue revealed tiny areas of focal necrosis, consisting of few degenerated hepatocytes and inflammatory cells at the higher dose level only.

Administration, Oral↗
PubMed1982

Neurochemical changes in rats coexposed to lead and copper.

Rats were coexposed to lead (Pb) and Copper (Cu) through drinking water and intraperitoneally, respectively, for a period of 21 days. Neurochemical studies in these rats showed significant reduction in the activity of adenosine triphosphatase, cytochrome-c-oxidase, diaphorase and in the levels of biogenic amines in the rats simultaneously exposed to the two metals compared to either of the metal alone. These neurotoxic effects were not related to the contents of either of the metals in the brain since their accumulation after combined exposure was much less than observed after individual exposure to Pb or Cu.

Adenosine Triphosphatases↗
PubMed1982

Effect of interaction of Mn2+ with Zn2+, Hg2+ and Cd2+ on some neurochemicals in rats.

Manganese chloride was administered alone or in combination with zinc chloride, mercuric chloride and cadmium chloride i.p. to rats daily for 30 days to investigate the effect of interaction of these elements on the contents of aromatic amino acids, biogenic amines and 5-hydroxyindole acetic acid (5-HIAA) in the brain. Combined manganese (Mn) and zinc (Zn) administration had an antagonistic effect on the contents of aromatic amino acids, but no effect on dopamine (DA) and produced a significant decrease in the content of 5-hydroxytryptamine (5-HT). Combination of Mn with mercury (Hg) or cadmium (Cd) produced pronounced changes in these neurochemicals indicating a more serious effect on the brain compared with a single treatment with either metal.

Animals↗
PubMed1982

Effects of manganese on carbohydrate metabolism and mitochondrial enzymes in rats.

The effect of daily intraperitoneal administration of Mn2+(4 mg/kg) was investigated on the metabolism of carbohydrates and certain enzymes involved in the oxidation of glucose in the rat liver and blood at the intervals of 30, 60 and 90 days after exposure. Mn2+ had no effect on the contents of blood reducing sugars and proteins, however the levels of pyruvic and lactic acids were reduced at 60 and 90 days after the metal treatment. The contents of liver glycogen and proteins remained unaffected while pyruvic acid content was decreased in Mn2+ treated rat liver throughout the experimental period. The activities of glycogen phosphorylase and lactate dehydrogenase decreased while that of phosphoglucoisomerase and glucose-6-phosphatase increased in the post mitochondrial supernatant at 60 and 90 days of Mn2+ exposure. The levels of hexokinase decreased and FDP-aldolase and fructose-1, 6-diphosphatase increased throughout the experimental period. The magnitude of alteration was found to be greater with the increase in the duration of Mn2+ treatment. Several of the mitochondrial enzymes in the liver were inhibited in the manganese exposed rats which may be responsible to inhibit the rate of dehydrogenation of Kreb cycle's intermediates along with the linked respiratory chain and eventually oxidation in the rat liver.

Animals↗