ascorbic-acid and nickel-sulfate

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 Wistar 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.

Topics: Animals; Ascorbic Acid; Lung; Male; Nickel; Nitric Oxide; Nitric Oxide Synthase Type II; Rats; Reactive Nitrogen Species; Stress, Physiological

To evaluate the alteration of chemical behavior of L-ascorbic acid (vitamin C) with metal ion (nickel) at different pH solutions in vitro.. 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.. 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.. 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.

Topics: Ascorbic Acid; Hydrogen-Ion Concentration; Nickel; Spectrum Analysis

Heavy metals generate free radicals and induce oxidative and nitrosative stress with depletion of antioxidants. In this study, we have evaluated the beneficial effects of α-tocopherol against nickel sulfate exposed testicular dysfunction.. We studied the effect of supplementation of α-tocopherol (10 mg/100 g body weight, i.m.) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced testicular oxidative and nitrosative stress in Wister strain male albino rats. Serum and testicular nitric oxide, L-ascorbic acid and serum α-tocopherol concentrations were evaluated. We also evaluated sperm count, motility and histopathology of testes.. Nickel treated rats showed significantly decreased body weight, testicular somatic index, sperm count, sperm motility, serum and testicular L-ascorbic acid concentration and serum α-tocopherol level as compared to their controls. However, simultaneous treatment with nickel sulfate and α-tocopherol produced a remarkable improvement of all the above parameters when compared with treatment with nickel alone. Nickel treated rats also had significantly increased serum and testicular nitric oxide concentrations as compared to their controls. However, simultaneous treatment with nickel sulfate and α-tocopherol significantly decreased nitric oxide concentrations in both serum and testes, respectively, as compared to nickel treatment alone. Histopathology of the testes revealed tortuous seminiferous tubules, loss of spermatogenesis process (>75%), congestion and necrosis in nickel sulfate treated rats, whereas rats simultaneously treated with nickel sulfate and α-tocopherol had almost normal seminiferous tubules and near normal spermatogenesis as compared to nickel alone treated rats.. Nickel sulfate treatment causes testicular oxidative and nitrosative stress in albino rats, but simultaneous supplementation of α-tocopherol was found to be beneficial in combating against such stresses.

Topics: alpha-Tocopherol; Animals; Antioxidants; Ascorbic Acid; Male; Nickel; Nitric Oxide; Oxidative Stress; Rats; Rats, Wistar; Seminiferous Tubules; Spermatogenesis; Testis

We evaluated the effect of L-ascorbic acid and alpha-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 alpha-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 alpha-tocopherol. Lead-treated animals showed a greater improvement with alpha-tocopherol, whereas nickel-treated rats showed a greater improvement with L-ascorbic acid. In both groups, combined supplementation with L-ascorbic acid and alpha-tocopherol did not change the percentage improvement in comparison with supplementation with a single vitamin alone.

Topics: alpha-Tocopherol; Animals; Antioxidants; Ascorbic Acid; Brain; Catalase; Glutathione Peroxidase; Lipid Peroxidation; Male; Nickel; Nitric Oxide; Organ Size; Organometallic Compounds; Rats; Superoxide Dismutase

We recently reported that induction of metallothionein (MT) was critical in limiting nickel (Ni)-induced lung injury in intact mice. Nonetheless, the mechanism by which Ni induces MT expression is unclear. We hypothesized that the ability of Ni to mobilize zinc (Zn) may contribute to such regulation and therefore, we examined the mechanism for Ni-induced MT2A expression in human airway epithelial (BEAS-2B) cells. Ni induced MT2A transcript levels and protein expression by 4 hours. Ni also increased the activity of a metal response element (MRE) promoter luciferase reporter construct, suggesting that Ni induces MRE binding of the metal transcription factor (MTF-1). Exposure to Ni resulted in the nuclear translocation of MTF-1, and Ni failed to induce MT in mouse embryonic fibroblasts lacking MTF-1. As Zn is the only metal known to directly bind MTF-1, we then showed that Ni increased a labile pool of intracellular Zn in cells as revealed by fluorescence-activated cell sorter using the Zn-sensitive fluorophore, FluoZin-3. Ni-induced increases in MT2A mRNA and MRE-luciferase activity were sensitive to the Zn chelator, TPEN, supporting an important role for Zn in mediating the effect of Ni. Although neither the source of labile Zn nor the mechanism by which Ni liberates labile Zn was apparent, it was noteworthy that Ni increased intracellular reactive oxygen species (ROS). Although both N-acetyl cysteine (NAC) and ascorbic acid (AA) decreased Ni-induced increases in ROS, only NAC prevented Ni-induced increases in MT2A mRNA, suggesting a special role for interactions of Ni, thiols, and Zn release.

Topics: Acetylcysteine; Animals; Antioxidants; Ascorbic Acid; Bronchi; Cell Separation; Cells, Cultured; Chelating Agents; Chlorides; DNA-Binding Proteins; Epithelial Cells; Ethylamines; Flow Cytometry; Fluorescent Dyes; Humans; Metallothionein; Mice; Mice, Knockout; Nickel; Polycyclic Compounds; Pyridines; Pyrimidines; Reactive Oxygen Species; RNA, Messenger; Time Factors; Transcription Factor MTF-1; Transcription Factors; Transcriptional Activation; Transfection; Up-Regulation; Zinc Compounds

In this experimental study, we investigated whether L-ascorbic acid has any influence on the blood antioxidant defense system, lipid peroxidation and hematological parameters of the albino rats exposed to nickel sulfate(NiSO4). Twenty four adult rats were divided into four groups of six animals in each group. The control rats were untreated and comprised Group I. Group II rats were administered nickel sulfate (2.0 mg/100 g b.wt.; intraperitonially, i.p.). Group II rats were treated orally L-ascorbic acid (50 mg/100 g b.wt.) and Group IV rats were given both nickel sulfate and L-ascorbic acid simultaneously on alternate days until the tenth dose. The hematological parameters were assessed: red blood corpuscle counts, packed cell volume %, hemoglobin concentration, white blood corpuscle counts and platelets count decreased significantly and clotting time increased significantly in nickel treated rats. We also observed increase malondialdehyde (MDA) and decrease glutathione level (GSH) in erythrocytes of nickel treated rats. The activities of erythrocyte antioxidant enzymes like superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) were significantly increased in rats treated with nickel sulfate. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on the hematological values, erythrocyte MDA and GSH concentrations as well as antioxidant enzymatic defense system.

Topics: Animals; Antioxidants; Ascorbic Acid; Erythrocytes; Injections, Intraperitoneal; Irritants; Lipid Peroxidation; Male; Nickel; Rats; Rats, Wistar

We studied the effect of oral supplementation with L-ascorbic acid (50 mg/100 g body weight) on nickel sulfate (2.0 mg/100 g body weight, i.p.) induced lipid peroxidation in the testes of Wister strain male albino rats. Testicular lipid peroxide and glutathione (GSH) levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GSH-Px) were estimated. Nickel sulfate treatment significantly increased the level of testicular lipid peroxide and decreased all antioxidant enzymes activities and GSH concentration. Simultaneously treatment of L-ascorbic acid exhibited a possible protective role on the toxic effect of nickel sulfate on testicular lipid peroxide and GSH concentration as well as antioxidant enzymatic defense system.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Catalase; Glutathione; Glutathione Peroxidase; Injections, Intraperitoneal; Lipid Peroxidation; Lipid Peroxides; Male; Nickel; Rats; Rats, Wistar; Sperm Count; Sperm Motility; Spermatozoa; Superoxide Dismutase; Testis

We studied the effect of oral supplementation with L-ascorbic acid (50 mg /100 g body weight (BW) on nickel sulfate (2.0 mg/ 100 g BW, i.p)-induced lipid peroxidation and histopathology in the lung of Wister strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes, superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px), were estimated. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased all antioxidant enzyme activities. Nickel sulfate treatment also induced (a) loss of normal characteristics and architectural organization, (b) inflammation in bronchioles, (c) alveolar congestion, (d) alveolar cell hyperplasia, and (e) congestion in the lumen. The simultaneous administration of L-ascorbic acid and nickel sulfate improved both lipid peroxidation and the histopathology of lung when compared with rats receiving nickel sulfate alone. The results indicate that L-ascorbic acid prevents nickel-induced alteration of antioxidant defense mechanisms and histopathology of lung tissue.

Topics: Animals; Antioxidants; Ascorbic Acid; Catalase; Glutathione Peroxidase; Lipid Peroxidation; Lung; Lung Diseases; Male; Necrosis; Nickel; Paraffin Embedding; Rats; Rats, Wistar; Superoxide Dismutase

We studied the effect of oral treatment with ascorbic acid (50 mg/100 g body weight) on nickel sulfate-induced (2.0 mg/100 g body weight, i.p.) alteration of nucleic acids and total protein concentration in the liver of Wistar strain male albino rats. Nucleic acids and total protein concentrations in treated rats decreased significantly when compared with untreated controls. The simultaneous administration of ascorbic acid with nickel sulfate resulted in a remarkable improvement of nucleic acids and total protein concentrations in liver in comparison with rats treated with nickel sulfate only. The results indicate that nickel influences the expression of genetic information by reducing hepatic DNA, RNA, and protein concentration in animals. Simultaneous treatment with ascorbic acid was beneficial for fighting against nickel-induced hepatoxicity.

Topics: Administration, Oral; Animals; Ascorbic Acid; Liver; Male; Nickel; Nucleic Acids; Rats; Rats, Wistar

We studied the effect of oral ascorbic acid treatment on nickel sulfate-induced lipid peroxidation in the liver of Wistar strain male albino rats. Lipid peroxide and glutathione levels and the activities of the antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) were estimated in liver. Nickel sulfate administration significantly increased the level of lipid peroxides and decreased glutathione, SOD, CAT, and GSH-Px activities in liver. The simultaneous administration of ascorbic acid with nickel sulfate resulted in a remarkable improvement of lipid peroxide, glutathione, SOD, CAT, and GSH-Px status in liver in comparison with rats treated with nickel alone. Nickel sulfate has an adverse effect on hepatic lipid peroxidation in animals, but simultaneous treatment with ascorbic acid offers a relative protection against nickel-induced hepatotoxicity.

Topics: Administration, Oral; Animals; Antioxidants; Ascorbic Acid; Catalase; Glutathione Peroxidase; Injections, Intraperitoneal; Lipid Peroxidation; Liver; Male; Nickel; Rats; Rats, Wistar; Superoxide Dismutase