Co-relation of trace elements in drinking water and soil.
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Copper↗
Biomedical subjects
R Nath
Publications and source records attributed to R Nath.
Absorption of glyoxylate and oxalate in thiamine and pyridoxine deficient rat intestine.
Dietary deficiency of thiamine or pyridoxine has been shown to produce hyperoxaluria and renal stone formation in man and experimental animals. To determine the possible contribution of exogenous glyoxylate and oxalate, the intestinal transport of [14C] - oxalate and [14C] - glyoxylate was measured in vitamin B1 and B6 deficient rats and their respective pair-fed controls. Results indicate that glyoxylate and oxalate are passively diffused from lumen to lamina propria in thiamine deficient and their pair-fed controls with no significant change in the rate of uptake of both the substrates. However B6 deficient rats showed a significant enhancement in the rate of oxalate uptake due to development of a new biphasic transport system. The rate of glyoxylate uptake by simple passive diffusion remained unaltered in pyridoxine deficiency.
Animals↗
Normalization of urinary oxalate by taurine in glycolate-fed rats.
Oral feeding of sodium glycolate (50 mg/d/rat for ten days) caused a significant (P less than 0.001) increase in oxalate and taurine excretion and a decrease in liver protein content (P less than 0.05), glycolic acid oxidase levels (P less than 0.01), and glycolic acid dehydrogenase levels (P less than 0.01) as compared to normal untreated rats. Taurine (100 mg/d/rat), when administered along with glycolate, prevented these effects of glycolate as evident from normal urinary excretion of oxalate, liver protein content, glycolic acid oxidase, and glycolic acid dehydrogenase levels in glycolate- plus taurine-fed animals.
Alcohol Oxidoreductases↗
A nonimmunomodulatory effect of chronic cadmium exposure on lymphocyte transformation response in rhesus monkeys (Macaca mulatta).
The immunomodulatory effects of cadmium, an environmental pollutant, were assessed in male rhesus monkeys orally exposed to 5 mg cadmium/kg body weight for a period of 4 months. A lymphocyte transformation test was carried out in peripheral blood lymphocytes using different concentrations of phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM). Cadmium exposure of monkeys resulted in a statistically nonsignificant increase in [3H]thymidine incorporation in PHA- and Con-A-stimulated lymphocytes. However, there was a nonsignificant decrease in [3H]thymidine incorporation in PWM-stimulated lymphocytes. These results suggest that cadmium may not have immunosuppressive effects in primates which are phylogenetically close to man.
Animals↗
Effect of protein calorie malnutrition and calcium deficiency on hepatic iso-metallothioneins in Cd-exposed monkeys.
Oral administration of cadmium results in the induction of metallothionein in liver of rhesus monkeys subjected to protein calorie malnutrition and calcium deficiency. Metallothionein was resolved into three iso-proteins viz. MTa, MTb & MTc which varied in their quantities and metal composition in these nutritional stress conditions. 'MTc' was the major iso-protein in protein calorie malnourished monkeys, while 'MTb' predominated in the calcium deficient group.
Animals↗
Effect of dietary chronic cadmium exposure on cell-mediated immune response in rhesus monkeys (Macaca mulatta): role of calcium deficiency.
The role of Ca deficiency on the immunomodulatory effects of chronic Cd exposure for a period of 10 weeks in male Rhesus monkeys were assessed by the blastogenic capacity of peripheral blood lymphocytes (PBL) in response to T-cell mitogens, phytohemagglutinin (PHA), and concanavalin A (Con A). Calcium deficiency significantly decreased the blastogenic response to PHA (P less than 0.01) and Con A (P less than 0.05). Although Cd exposure in normal monkeys significantly increased the blastogenic response to Con A (P less than 0.05), Cd exposure in Ca-deficient monkeys produced a further significant decrease in the blastogenic response to Con A (P less than 0.001). Total and ionic Ca were also significantly decreased in plasma of Ca deficient monkeys exposed to Cd. It is possible that these two observations may be related to each other. Thus, it is important to assess the nutritional status of the host while evaluating the immunotoxicological effects of an environmental pollutant.
Animals↗
Effect of pyridoxine deficiency on intestinal absorption of calcium and oxalate: chemical composition of brush border membranes in rats.
[U-14C]oxalic acid and 45Ca uptake was measured in control and vitamin B6-deficient rats. Calcium and oxalate uptake rates were significantly increased from the intestine of vitamin B6-deficient rats as compared to pair-fed controls. Oxalate uptake in pair-fed control rats follows a passive diffusion. In pyridoxine-deficient rats, the oxalate uptake increases nonlinearly as the oxalate concentration in the incubation medium increased, indicating a two-component system--a saturable sodium-independent uptake and a linear nonsaturable passive-diffusion component. The brush border membrane composition reveals that membrane sialic acid, cholesterol, and protein contents were markedly reduced. These aberrations in the chemical composition of brush border membrane may be responsible for the enhanced oxalic acid uptake in vitamin B6-deficient rats.
Animals↗
Effect of estradiol on the oxalate metabolism in vitamin B6-deficient male rats.
Estradiol-implanted (EB) and sham-operated (SB) male rats (100-120 g Fody wt) were kept on a vitamin B6-deficient diet for 1 month along (Formula: see text) with their respective estradiol pair-fed (EPF) and sham-operated pair-fed (SPF) controls. Pyridoxine-deficient animals had higher kidney weights and increased activities of liver glycolic acid oxidase (GAO) and glycolic acid dehydrogenase (GAD) as compared to their pair-fed control animals. Kidney weights, GAO, and GAD levels in these animals are negatively correlated with erythrocyte alanine transaminase (EALT) levels, indicating that pyridoxine status regulates these two major enzymes of oxalate biosynthesis. Estradiol-treated animals showed a lower reduction in EALT levels after feeding them a pyridoxine-deficient diet for 1 month as compared to untreated animals. Estradiol administration decreased GAO levels in both normal and pyridoxine-deficient animals.
Alanine Transaminase↗
Sodium glycolate absorption in rat intestine.
Absorption of sodium [1-14C]glycolate by rat intestine was studied by using the tissue accumulation technique with everted intestinal rings. Saturation kinetics was observed for the absorption of glycolate in the jejunoileal region, with a Km of 6.25 mM for glycolate and a Vmax of 5.56 mumole/30 min/g wet wt. The absorption was linear up to a period of 25 min at 37 degrees C. Jejunum and ileum showed significantly higher absorption of glycolate as compared to colon. Sulfhydryl binding agents, viz., p-chloromercuribenzoate and iodoacetate, and respiration inhibitors, e.g., KCN and 2,4-dinitrophenol, had no significant effect on glycolate uptake. However, glyoxylate and lactate showed significant inhibition at 6 mM concentration of the inhibitor. Pyridoxine deficiency had no effect on glycolate uptake by the rat intestine.
2,4-Dinitrophenol↗
Molecular aspects of idiopathic urolithiasis.
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Adult↗
Cadmium an inhibitor of lymphocyte transformation and stimulator of antibody-dependent cell-mediated cytotoxicity (ADCC) in rats: the role of zinc.
The effect of zinc (Zn) on the immunomodulatory properties of cadmium (Cd) was investigated in male Wistar rats. Animals were orally exposed to Cd and or Zn, by stomach tubing for 7 weeks. Response of splenocytes to phytohemagglutinin (PHA) and concanavalin A (Con A), was significantly increased by Zn. When exposed in combination with Cd, Zn restored the inhibitory effects of Cd on lymphocyte transformation. However, Cd significantly increased the antibody-dependent cell-mediated cytotoxic (ADCC) activity of the splenocytes on chicken red blood cells (CRBC). Zn had no effect on ADCC, nor did it modify the ADCC changes mediated by Cd.
Administration, Oral↗
Effect of dietary chronic cadmium exposure on cell-mediated immune response in rhesus monkey (Macaca mulatta).
Rhesus monkeys (Macaca mulatta) were daily exposed orally to cadmium (Cd) at 5 mg/kg body wt in diet for a period of 2 and 6 months. Significant amount of Cd accumulated in liver, kidney and spleen after its exposure to monkeys. Cell mediated immune response was assessed by the responsiveness of peripheral blood lymphocytes (PBL) to phytohemagglutinin (PHA), concanavalin A (Con A) and pokeweed mitogen (PWM). Even after 6 months of exposure, Cd increased DNA synthesis, although not significantly, in unstimulated and mitogen stimulated lymphocytes. Stimulation Index (SI), however, decreased largely due to increased unstimulated [( 3H]thymidine incorporation) observed after Cd exposure. It, therefore, indicates that Cd is not immunosuppressive in primates, phylogenetically closer to humans.
Animals↗
Induction of Cd-metallothionein in cadmium exposed monkeys under different nutritional stresses.
Induction of cadmium metallothionein (MT) in chronic cadmium exposure in Rhesus monkeys undergoing protein calorie malnutrition (PCM) and calcium deficiency has been studied. A positive correlation between cadmium content and levels of MT in kidney, liver, intestine, testis, heart and lung, has been observed. The accumulation of cadmium and synthesis of MT in these tissues was highest in monkeys subjected to cadmium exposure during calcium deficiency. Although more of cadmium is directed towards kidneys of calcium-deficient monkeys the MT-inducing ability of kidney is lower than that of liver. Monkeys on PCM diet also showed enhanced accumulation of cadmium and MT as compared to those on normal diet during cadmium exposure.
Animals↗
Molecular basis of cadmium toxicity.
Cadmium has been shown to manifest its toxicity in human and animals by mainly accumulating in almost all of the organs and kidney is the main target organ where it is concentrated mainly in cortex. Environmental exposure of cadmium occurs via food, occupational industries, terrestrial and aquatic ecosystem. At molecular level, cadmium interferes with the utilization of essential metals e.g. Ca, Zn, Se, Cr and Fe and deficiencies of these essential metals including protein and vitamins, exaggerate cadmium toxicity, due to its increased absorption through the gut and greater retention in different organs as metallothionein (Cd-Mt). Cadmium transport, across the intestinal and renal brush border membrane vesicles, is carrier mediated and it competes with zinc and calcium. It has been postulated that cadmium shares the same transport system. Cadmium inhibits protein synthesis, carbohydrate metabolism and drug metabolizing enzymes in liver of animals. Chronic environmental exposure of cadmium produces hypertension in experimental animals. Functional changes accompanying cadmium nephropathy include low molecular weight proteinuria which is of tubular origin associated with excess excretion of proteins such as beta 2 microglobulin, metallothionein and high molecular weight proteinuria of glomerular origin (excretion of proteins such as albumin IgG, transferrin etc.). Recent data has shown that metallothionein is more nephrotoxic to animals. Cadmium is also toxic to central nervous system. It causes an alterations of cellular functions in lungs. Cadmium affects both humoral and cell mediated immune response in animals. Cadmium induces metallothionein in liver and kidney but under certain nutritional deficiencies like protein-calorie malnutrition and calcium deficiency, enhanced induction and greater accumulation of cadmium metallothionein has been observed.
Aging↗
Intestinal oxalate uptake in castrated male and female rats: evidence for altered brush border membrane composition.
The intestinal uptake rate of oxalate (mumoles/h/g tissue wt.) in castrated male (CM) rats, CM rats administered estradiol, and female (F) rats was 1.8, 1.4 and 1.3 times higher than that of male rats, whereas castrated female (CF) rats and CF rats administered testosterone absorbed oxalate at a rate similar to F rats, thereby, suggesting that gonadectomy affected intestinal uptake of oxalate only in male rats The intestinal oxalate uptake rate in all the groups increased linearly with increasing oxalate concentration (0.1- 6.0 mM). Chemical composition of brush border membrane showed significant changes in the sialic acid, phospholipid and cholesterol content following castration, which may lead to ultrastructural changes in the membrane thereby, increasing the absorption of oxalate.
Animals↗
Evidence of increased intestinal absorption of oxalate in rats induced for bladder stone.
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Animals↗
Effect of sodium glycolate and sodium pyruvate on oxalic acid biosynthesizing enzymes in rat liver and kidney.
Sodium glycolate feeding (50 mg/100 g body weight/day) to adult male rats for 7 days resulted in increased activities of glycolate oxidase in liver and lactate dehydrogenase in liver and kidney. However, the activity of glycolate dehydrogenase decreased both in liver and kidney. Treatment of sodium pyruvate (100 mg/100 g body weight/day) to the glycolate-fed rats resulted in lowered liver glycolate oxidase activity, and the glycolate dehydrogenase activity was further decreased as compared to glycolate-fed rats in both age groups. However, lactate dehydrogenase activity was not affected by pyruvate feeding in comparison to the glycolate-treated group. It is concluded that glycolate-induced oxalate biosynthesis in rats involves increased activity of liver glycolate oxidase, and pyruvate feeding inhibits glycolate oxidase, thereby decreasing oxalate biosynthesis.
Alcohol Oxidoreductases↗
Intestinal absorption of oxalate in scorbutic and ascorbic acid supplemented guinea pigs.
Radiolabelled U-14C oxalic acid uptake was measured in the intestine of scorbutic and ascorbic acid (AA) supplemented guinea pigs. The feeding of vitamin C deficient diet to the animals for 26 days resulted in a significant fall in the ascorbic acid levels in the various tissues studied. Supplementation of vitamin C (10, 25 or 50 mg per 200 g body weight) increased ascorbic acid levels of spleen, adrenals, liver and leucocytes. The intestinal uptake of oxalate follows a passive diffusion mechanism in normally fed guinea pigs. The oxalate uptake rate was significantly increased (p less than 0.001) in the vitamin C administered group. Vitamin C depletion significantly decreased the oxalate uptake rate as compared to control animals. The changes observed in the uptake rate appear to be related with the chemical aberrations produced in the brush border membranes.
Animals↗