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Copper (Cu) is a heavy metal that is widely used in industries and is also an essential micronutrient for living beings. However, excess Cu is toxic and human exposure to high levels of this metal results in numerous adverse health effects. We have investigated the effect of oral administration of copper chloride (CuCl

Sodium chlorate (NaClO

Sodium nitrite (NaNO2 ) is widely used as a food additive and preservative in fish and meat products. We have evaluated the effect of a single acute oral dose of NaNO2 on oxidative stress parameters, antioxidant capacity, and DNA in rat kidney. Male Wistar rats were divided into four groups and given single oral dose of NaNO2 at 20, 40, 60, and 75 mg/kg body weight; untreated rats served as the control group. All animals in NaNO2 -treated groups showed marked alterations in various parameters of oxidative stress as compared to the control group. This included increase in lipid peroxidation, protein oxidation, hydrogen peroxide levels, and decrease in reduced glutathione content and antioxidant capacity. Administration of NaNO2 also increased DNA damage as evident from release of free nucleotides and confirmed by comet assay. It also led to greater cross-linking of DNA to proteins. Histological analysis showed marked morphological changes in the kidney of NaNO2 -treated animals. These alterations could be due to increased free radical generation or direct chemical modification by reaction intermediates. Our results suggest that nitrite-induced nephrotoxicity is mediated through redox imbalance and results in DNA damage.

Nitrite is present as a noxious contaminant in drinking water and causes oxidative damage in various tissues of humans and animals. It is a well-known methemoglobin-forming agent that has been shown to damage blood cells. The protective effect of taurine, a semi-essential sulfur-containing amino acid, was studied on sodium nitrite (NaNO2)-induced oxidative damage in human erythrocytes. Erythrocytes were incubated with NaNO2, in the presence and absence of taurine, and changes in oxidative stress parameters determined. Pretreatment with taurine significantly ameliorated NaNO2-induced oxidative damage to lipids, proteins, and plasma membrane. It also reduced the NaNO2-induced increase in methemoglobin levels and ROS production. Taurine improved the antioxidant capacity of cells, restored the alterations in the activities of various metabolic enzymes, and prevented morphological changes in erythrocytes. Thus, taurine can be potentially used as a protective agent against the damaging effects of nitrite.

Sodium chlorate (NaClO3) is widely used in paper and pulp industries and as a non-selective herbicide. It is also a major by-product generated upon disinfection of drinking water by chlorine dioxide. In this study, we have investigated the genotoxicity of NaClO3 on the small intestine of rats. Adult male rats were divided into 5 groups: one control and four NaClO3 treated groups. The NaClO3 treated groups were given a single acute oral dose of NaClO3 (100, 250, 500 and 750 mg/kg body weight) and sacrificed 24 h later. Administration of NaClO3 caused significant DNA damage in a dose dependent manner in the rat intestine. This was evident from the comet assay which showed DNA strand breaks and was further confirmed by agarose gel electrophoresis and release of free nucleotides. Increased DNA protein cross-linking in NaClO3 administered groups showed formation of a critical lesion which hampers activities of proteins/enzymes involved in DNA repair, transcription and replication. Thus, oral administration of NaClO3 induces DNA damage in the rat intestine, probably through chlorate induced production of reactive oxygen species.

Sodium chlorate (NaClO3 ) is a widely used nonselective herbicide. It is also generated as a by-product during disinfection of drinking water by chlorine dioxide. The purpose of this study was to evaluate the effect of NaClO3 on rat intestine. Adult male rats were randomly divided into five groups: control and remaining four groups were administered orally different doses of NaClO3 and sacrificed 24 h after the treatment. The administration of NaClO3 produced acute oxidative stress in the intestine, which manifested in the form of markedly enhanced malondialdehyde levels and carbonyl content and lowered total sulfhydryl groups and glutathione levels. The activities of several brush border membrane (BBM) enzymes were greatly reduced as compared to control. There were alterations in the activities of various enzymes of carbohydrate metabolism and those involved in maintaining the antioxidant defense system. Histological studies support the biochemical results showing NaClO3 dose-dependent increase in tissue damage. Thus, the present study shows that oral administration of NaClO3 decreases the activities of BBM enzymes, induces oxidative stress, alters metabolic pathways, and impairs the antioxidant system of rat intestine. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1607-1616, 2017.

Sodium nitrite (NaNO2) is a common contaminant of drinking water and food and feed chain. Nitrite induces oxidative damage in humans and animals. In this work we studied the protective effect of crocin, the active constituent of Crocus sativus (saffron), on NaNO2-induced oxidative damage in human erythrocytes. Changes in oxidative stress parameters following NaNO2 incubation of erythrocytes in presence and absence of crocin were determined. It was found that crocin pre-treatment significantly attenuated NaNO2-induced oxidative damage of proteins, lipids and plasma membrane. Crocin reduced the level of methemoglobin, the primary acute effect of nitrite intoxication. It also improved the antioxidant capacity of cells and NaNO2-induced morphological changes in erythrocytes. Crocin is thus a potent protective agent against nitrite-induced cytotoxicity.

Sodium chlorite (NaClO2 ) is used in the production of chlorine dioxide for bleaching and stripping of textiles, pulp, and paper. It is also used as disinfectant in municipal water treatment and as a component in therapeutic rinses and gels. The effect of NaClO2 on human erythrocytes has been studied under in vitro conditions. Incubation of 5% suspension of erythrocytes with NaClO2 (0.1-2.0 mM) at 37°C for 30 min resulted in marked cell lysis (1.2-3.8 fold) and increased their osmotic fragility. Several parameters were assayed in cell lysates prepared from NaClO2 -treated and -untreated (control) erythrocytes. Compared to controls, exposure to NaClO2 caused significant increase in protein oxidation (1.1-8.07 fold), lipid peroxidation (1.08-4.95 fold) with decrease in total sulfhydryl (-5 to -61%), and glutathione levels (-7 to -86%). Methemoglobin content was tremendously increased, by 5-52 fold when compared to control, while methemoglobin reductase activity decreased (-17 to -93%) upon NaClO2 treatment. NaClO2 enhanced the generation of reactive oxygen species by 3-21 fold and lowered the metal reducing and free radical quenching ability of erythrocytes. It also caused an increase in nitric oxide levels (2.7-15.4 fold) showing generation of nitrosative stress too. The activities of major antioxidant and membrane bound enzymes were significantly altered. Gross morphological changes, from discocytes to echinocytes, were seen in NaClO2 -treated erythrocytes under electron microscope. These results show that NaClO2 induces oxidative stress in human erythrocytes, damages the membrane, and impairs the cellular antioxidant defence system. This oxidative damage can shorten the life span of erythrocytes in blood resulting in red cell senescence. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1343-1353, 2017.

Sodium chlorate (NaClO3 ) is widely used in paper and pulp industries and as a non-selective herbicide. Humans can be exposed to NaClO3 through contaminated drinking water due to its improper and unchecked usage in industries and as herbicide. NaClO3 is also present as a major stable by-product in drinking water that has been disinfected with chlorine dioxide. In this study, we have investigated the effect of a single acute oral dose of NaClO3 on rat kidney. Adult male Wistar rats were divided into one control and four NaClO3 treated groups that were orally given different doses of NaClO3 and euthanized 24 hr after the treatment. Oral administration of NaClO3 resulted in increased hydrogen peroxide levels, lipid, and protein oxidation while thiol and glutathione content and activities of brush border membrane enzymes were decreased in kidney in a NaClO3 dose-dependent manner. Significant alterations in the activities of enzymes involved in carbohydrate metabolism and antioxidant defense were also observed. Administration of NaClO3 induced DNA fragmentation and increased DNA-protein cross-linking. Histological studies showed marked damage in kidney from NaClO3 treated animals. These results strongly suggest that NaClO3 induces nephrotoxicity via redox imbalance that results in DNA and membrane damage, metabolic alterations and brush border membrane enzyme dysfunction.

Industrialization and unchecked use of nitrate/nitrite salts for various purposes has increased human exposure to high levels of sodium nitrite (NaNO2) which can act as a pro-oxidant and pro-carcinogen. Oral exposure makes the gastrointestinal tract particularly susceptible to nitrite toxicity. In this work, the effect of administration of a single acute oral dose of NaNO2 on rat intestine was studied. Animals were randomly divided into four groups and given single doses of 20, 40, 60 and 75 mg NaNO2/kg body weight. Untreated animals served as the control group. An NaNO2 dose-dependent decline in the activities of brush border membrane enzymes, increase in lipid peroxidation, protein oxidation, hydrogen peroxide levels and decreased thiol content was observed in all treated groups. The activities of various metabolic and antioxidant defense enzymes were also altered. NaNO2 induced a dose-dependent increase in DNA damage and DNA-protein crosslinking. Histopathological studies showed marked morphological damage in intestinal cells. The intestinal damage might be due to nitrite-induced oxidative stress, direct action of nitrite anion or chemical modification by reaction intermediates.

Sodium chlorate (NaClO

Sodium chlorite (NaClO

Sodium chlorate (NaClO3) is a widely used non-selective herbicide. It is also generated as a byproduct during disinfection of drinking water by chlorine dioxide. In the present work, the effects of NaClO3 on human erythrocytes were studied under in vitro conditions. Incubation of erythrocytes with different concentrations of NaClO3 at 37 °C for 90 min resulted in significant hemolysis. Cell lysates were prepared from NaClO3-treated and untreated (control) erythrocytes and assayed for various biochemical parameters. Methemoglobin levels were significantly increased and methemoglobin reductase activity was reduced upon NaClO3 treatment. There was a significant increase in protein oxidation and lipid peroxidation with a decrease in reduced glutathione and total sulfhydryl content. This suggests the induction of oxidative stress in erythrocytes upon exposure to NaClO3. The occurrence of oxidative stress was confirmed by significantly increased generation of reactive oxygen species and lowered antioxidant response of the cells. NaClO3 treatment also increased nitric oxide levels showing induction of nitrosative stress. The activities of major antioxidant and membrane-bound and metabolic enzymes were significantly altered upon incubation of erythrocytes with NaClO3. The erythrocytes became more osmotically fragile while electron microscopic images showed gross morphological alterations in NaClO3-treated cells. These results show that NaClO3 induces oxidative stress in human erythrocytes, which results in extensive membrane damage and lowers the antioxidant response.

Nitrite salts are present as contaminants in drinking water and in the food and feed chain. In this work, the effect of sodium nitrite (NaNO2) on human erythrocytes was studied under in vitro conditions. Incubation of erythrocytes with 0.1-10.0 mM NaNO2 at 37 °C for 30 min resulted in dose dependent decrease in the levels of reduced glutathione, total sulfhydryl and amino groups. It was accompanied by increase in hemoglobin oxidation and aggregation, lipid peroxidation, protein oxidation and hydrogen peroxide levels suggesting the induction of oxidative stress. Activities of all major erythrocyte antioxidant defense enzymes were decreased in NaNO2-treated erythrocytes. The activities of enzymes of glycolytic and pentose phosphate pathways were also compromised. However, there was a significant increase in acid phosphatase and also AMP deaminase, a marker of erythrocyte oxidative stress. Thus, the major metabolic pathways of cell were altered. Erythrocyte membrane damage was suggested by lowered activities of membrane bound enzymes and confirmed by electron microscopic images. These results show that NaNO2-induced oxidative stress causes hemoglobin denaturation and aggregation, weakens the cellular antioxidant defense mechanism, damages the cell membrane and also perturbs normal energy metabolism in erythrocytes. This nitrite-induced damage can reduce erythrocyte life span in the blood.