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Das K.K.,Environmental Health Research Unit | Saha S.,University of Leeds
Journal of Basic and Clinical Physiology and Pharmacology | Year: 2010

We evaluated the effect of L-ascorbic acid and α-tocopherol supplementation on plasma and whole brain nitric oxide level and antioxidant status in nickel sulfate- or lead acetate- treated male albino rats. Nitric oxide and lipid peroxide levels in whole brain tissue and plasma increased following nickel and lead treatment but significantly returned to near-normal values upon L-ascorbic acid or α-tocopherol supplementation. In brain tissue, antioxidant enzymes - superoxide dismutase, glutathione peroxidase, glutathione peroxidase, and catalase - along with the glutathione level decreased significantly after both treatments but significantly improved upon simultaneous supplementation with L-ascorbic acid or α-tocopherol. Lead-treated animals showed a greater improvement with α-tocopherol, whereas nickel-treated rats showed a greater improvement with L-ascorbic acid. In both groups, combined supplementation with L-ascorbic acid and α-tocopherol did not change the percentage improvement in comparison with supplementation with a single vitamin alone. © 2010 Freund Publishing House Limited.

Jargar J.G.,Environmental Health Research Unit | Dhundasi S.A.,Environmental Health Research Unit | Das K.K.,Blde University Shri Bmpatil Medical College
Biomedicine (India) | Year: 2014

Introduction: There is growing evidence that oxidative stress contributes to the pancreatic islet P-cell destruction in diabetes. It seems that nickel induces glucose deregulation through reactive oxygen species (ROS) pathway. Since vitamin E is known to protect the cells from oxidative damage due to its potent antioxidant properties.Aim: Role of a-tocopherol on blood glucose regulation in diabetic rats exposed to nickel sulfate were investigated.Materials and Methods: Group I served as normal control. Diabetes was induced in male albino rats (180-200g b.wt) with alloxan monohydrate (15mg/100g b.wt, i.p.). Group II diabetic control, Group III (diabetic + nickel sulfate, 2mg/100gb.wt, i.p.), Group IV (diabetic + a-tocopherol, 10mg/100gb.wt, i.m.) and Group V (diabetic + nickel sulfate+α-tocopherol).Results: The authors found that body weight gain, hepato and renal somatic index were significantly improved in hyperglycemic rats due to a-tocopherol supplementation. Chronic blood glucose level, oral glucose tolerance test (OGTT), serum nitric oxide (NO) and vitamin E levels were significantly increased in both diabetic and nickel sulfate exposed diabetic rats after a-tocopherol supplementation.Conclusion: a-Tocopherol supplementation exerts a protective influence on blood glucose regulation in diabetes and nickel sulfate exposed diabetes by attenuating hyperglycemia-mediated oxidative stress and antioxidant competence.

Das K.K.,Environmental Health Research Unit | Dhundasi S.A.,Environmental Health Research Unit | Das S.N.,Environmental Health Research Unit
Journal of Basic and Clinical Physiology and Pharmacology | Year: 2011

Hexavalent chromium or chromium (VI) is a powerful epithelial irritant and a confirmed human carcinogen. This heavy metal is toxic to many plants, aquatic animals, and bacteria. Chromium (VI) which consists of 10%-15% total chromium usage, is principally used for metal plating (H 2Cr 2O 7), as dyes, paint pigments, and leather tanning, etc. Industrial production of chromium (II) and (III) compounds are also available but in small amounts as compared to chromium (VI). Chromium (VI) can act as an oxidant directly on the skin surface or it can be absorbed through the skin, especially if the skin surface is damaged. The prooxidative effects of chromium (VI) inhibit antioxidant enzymes and deplete intracellular glutathione in living systems and act as hematotoxic, immunotoxic, hepatotoxic, pulmonary toxic, and nephrotoxic agents. In this review, we particularly address the hexavalent chromium-induced generation of reactive oxygen species and increased lipid peroxidation in humans and animals, and the possible role of garlic (Allium sativum Linn) as a protective antioxidant. © 2011 by Walter de Gruyter Berlin Boston.

Maniyar S.A.,Environmental Health Research Unit | Jargar J.G.,Environmental Health Research Unit | Das S.N.,P.A. College | Dhundasi S.A.,Environmental Health Research Unit | Das K.K.,Environmental Health Research Unit
Asian Pacific Journal of Tropical Biomedicine | Year: 2012

Objective: To evaluate the alteration of chemical behavior of L-ascorbic acid (vitamin C) with metal ion (nickel) at different pH solutions in vitro. Methods: Spectra of pure aqueous solution of L-ascorbic acid (E mark) compound and NiSO4 (H2O) (sigma USA) were evaluated by UV visible spectrophotometer. Spectral analysis of L-ascorbic acid and nickel at various pH (2.0, 7.0, 7.4 and 8.6) at room temperature of 29°C. was recorded. In this special analysis, combined solution of L-ascorbic acid and nickel sulfate at different pH was also recorded. Results: The result revealed that. λmax (peak wavelength of spectra) of L-ascorbic acid at pH 2.0 was 289.0 nm whereas at neutral pH 7.0,. λmax was 295.4 nm. In alkaline pH 8.6, λmax was 295.4 nm and at pH 7.4 the. λmax of L-ascorbic acid remained the same as 295.4 nm. Nickel solution at acidic pH 2.0 was 394.5 nm, whereas at neutral pH 7.0 and pH 7.4 were the same as 394.5 nm. But at alkaline pH 8.6,. λmax value of nickel sulfate became 392.0 nm. The combined solution of L-ascorbic acid and nickel sulfate (6 mg/mL each) at pH 2.0 showed 292.5 nm and 392.5 nm, respectively whereas at pH 7.0, L-ascorbic acid showed 296.5 nm and nickel sulfate showed 391.5 nm. At pH 7.4, L-ascorbic acid showed 297.0 nm and nickel sulfate showed 394.0 nm in the combined solution whereas at pH 8.6 (alkaline) L-ascorbic acid and nickel sulfate were showing 297.0 and 393.5 nm, respectively. Conclusions: Results clearly indicate an altered chemical behavior of L-ascorbic acid either alone or in combination with nickel sulfate in vitro at different pH. Perhaps oxidation of L-ascorbic acid to L-dehydro ascorbic acid via the free radical (HSc*) generation from the reaction of H2ASc + Ni (II) is the cause of such alteration of. λmax value of L-ascorbic acid in the presence of metal nickel.

Hattiwale S.H.,Environmental Health Research Unit | Saha S.,University of Leeds | Yendigeri S.M.,Al Ameen Medical College | Jargar J.G.,Environmental Health Research Unit | And 2 more authors.
BioMetals | Year: 2013

Nickel sulfate stimulates inducible nitric oxide synthase (i-NOS) and increases serum nitric oxide concentration by overproduction of reactive nitrogen species due to nitrosative stress. The present study was undertaken to assess possible protective role of l-ascorbic acid as an antioxidant against nickel induced pulmonary nitrosative stress in male albino rats. We studied the effect of the simultaneous treatment with l-ascorbic acid (50 mg/100 g b. wt.; orally) and nickel sulfate (2.0 mg/100 g b. wt.; i.p.) on nitric oxide synthesis by quantitative evaluation of serum i-NOS activities, serum and lung nitric oxide, l-ascorbic acid and protein concentrations of Wister strain male albino rats. We have further studied histopathological changes in lung tissue after nickel sulfate treatment along with simultaneous exposure of l-ascorbic acid. Nickel sulfate treatment significantly increased the serum i-NOS activity, serum and pulmonary nitric oxide concentration and decreased body weight, pulmonary somatic index, serum and lung l-ascorbic acid and protein concentration as compared to their respective controls. Histopathological changes induced by nickel sulfate showed loss of normal alveolar architecture, inflammation of bronchioles, infiltration of inflammatory cells and patchy congestion of alveolar blood vessels. The simultaneous administration of l-ascorbic acid and nickel sulfate significantly improved all the above biochemical parameters along with histopathology of lung tissues of rats receiving nickel sulfate alone. The study clearly showed a protective role of l-ascorbic acid against nickel induced nitrosative stress in lung tissues. © 2013 Springer Science+Business Media New York.

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