<i>In vitro</i>kinetics of the oxidative reactivity of nitrate and nitrite in the rat erythrocyte

Batina, P.; Fritsch, P.; G, de Saint Blanquat; Mt, Mitjavila

doi:10.1080/02652039009373868

Cited by 14 publications

(10 citation statements)

References 8 publications

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“…The toxic effects of nitrite are thought to be mediated by the induction of oxidative stress. This is supported by observations that nitrite increases lipid peroxidation, protein oxidation, and lowers GSH levels in treated cells/tissues (Batina et al, 1990;Vossen and De Smet, 2015). Furthermore, antioxidant supplementation has been shown to alleviate nitrite toxicity (Al-Gayyar et al, 2014, 2016.…”

Section: Resultsmentioning

confidence: 74%

Sodium nitrite enhances generation of reactive oxygen species that decrease antioxidant power and inhibit plasma membrane redox system of human erythrocytes

Ansari

Mahmood

2016

Cell Biology International

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Nitrite/nitrate salts are used in fertilizers and as food preservatives. Human exposure to high levels of nitrite results in its uptake and subsequent entry into blood where it can interact with erythrocytes. We show that treatment of human erythrocytes with sodium nitrite (NaNO2 ) results in a dose-dependent increase in the production of reactive oxygen species. This was accompanied by a decrease in the antioxidant power which lowered the free radical quenching and metal-reducing ability. NaNO2 treatment also inhibited plasma membrane redox system (PMRS) of erythrocytes. These changes increase the susceptibility of erythrocytes to oxidative damage, decrease the antioxidant power of whole blood, and can be a major cause of nitrite-induced cellular toxicity.

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Section: Resultsmentioning

confidence: 74%

Sodium nitrite enhances generation of reactive oxygen species that decrease antioxidant power and inhibit plasma membrane redox system of human erythrocytes

Ansari

Mahmood

2016

Cell Biology International

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“…To determine whether increased levels of membrane-bound hemichromes might have affected the ZP of CC erythrocytes, we induced hemichromes and other hemoglobin degradation products in AA erythrocytes with sodium nitrite (NaNO 2 ). At certain concentrations, NaNO 2 promotes not only the peroxidation of lipids [57] but also the conversion of oxyhemoglobin (Fe 2+ ) to methemoglobin (Fe 3+ ) [58], [59], which spontaneously converts to hemichromes at a rate that depends on its own tertiary structure [60]. Treatment of AA erythrocytes with NaNO 2 increased hemichromes by 65% (1.03±0.29 for control AA vs. 1.68±0.18 for NaNO 2 -treated AA, n = 6, P = 0.0009) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Altered Membrane Structure and Surface Potential in Homozygous Hemoglobin C Erythrocytes

et al. 2009

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BackgroundHemoglobin C differs from normal hemoglobin A by a glutamate-to-lysine substitution at position 6 of beta globin and is oxidatively unstable. Compared to homozygous AA erythrocytes, homozygous CC erythrocytes contain higher levels of membrane-associated hemichromes and more extensively clustered band 3 proteins. These findings suggest that CC erythrocytes have a different membrane matrix than AA erythrocytes.Methodology and FindingsWe found that AA and CC erythrocytes differ in their membrane lipid composition, and that a subset of CC erythrocytes expresses increased levels of externalized phosphatidylserine. Detergent membrane analyses for raft marker proteins indicated that CC erythrocyte membranes are more resistant to detergent solubilization. These data suggest that membrane raft organization is modified in CC erythrocytes. In addition, the average zeta potential (a measure of surface electrochemical potential) of CC erythrocytes was ≈2 mV lower than that of AA erythrocytes, indicating that substantial rearrangements occur in the membrane matrix of CC erythrocytes. We were able to recapitulate this low zeta potential phenotype in AA erythrocytes by treating them with NaNO2 to oxidize hemoglobin A molecules and increase levels of membrane-associated hemichromes.ConclusionOur data support the possibility that increased hemichrome deposition and altered lipid composition induce molecular rearrangements in CC erythrocyte membranes, resulting in a unique membrane structure.

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“…Furthermore, nitrite anion accumulation in the erythrocytes can also influence the increase in membrane potential changes. The decrease in membrane fluidity may result, according to Batina et al, (), from the changes of the membrane structural state due to the membrane oxidative process provoking hemolysis. Nitrate‐induced oxidative reactivity alters cell ionic flux; leading to the osmotic fragility of the erythrocyte membrane as well as a perturbation of membrane transport that tends to hemolysis as reported by Bogard et al, ().…”

Section: Discussionmentioning

confidence: 99%

Hyparrhenia hirta: A potential protective agent against hematotoxicity and genotoxicity of sodium nitrate in adult rats

Bouaziz‐Ketata

Salah

Mahjoubi

et al. 2014

Environmental Toxicology

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The present study was carried out to examine the adverse hematotoxic and genotoxic effects of water nitrate pollution on male adult rats and the use of hyparrhenia hirta methanolic extract in alleviating these effects. Sodium nitrate (NaNO3 ) was administered to adult rats by oral gavage at a dose of 400 mg kg(-1) bw daily for 50 days, while hyparrhenia hirta methanolic extract was given by drinking water at a dose of 1.5 mg mL(-1) (200 mg kg(-1) bw). The NaNO3 -treated group showed a significant decrease in red blood cell count, hemoglobin and hematocrit and a significant increase in total white blood cell, in neutrophil and eosinophil counts. Platelet count, mean corpuscular volume, mean corpuscular hemoglobin, and mean corpuscular hemoglobin concentration remained unchanged in treated groups compared to those of controls. Meanwhile, the results showed a marked reduction in the antioxidant enzyme activities, such as superoxide dismutase, catalase, and glutathione peroxidase, along with an elevation in the level of lipid peroxidation and a reduction in the total glutathione content, indicating the induction of oxidative stress in the erythrocytes of NaNO3 -treated group. Interestingly, NaNO3 treatment showed a significant increase in the frequencies of total chromosomal aberrations, aberrant metaphases and micronucleus in bone-marrow cells. The oxidative stress induced by nitrate treatment might be the major cause for chromosomal rearrangements as free radicals leading to DNA damage. Hyparrhenia hirta methanolic extract appeared to be effective against hematotoxic and genotoxic changes induced by nitrate, as evidenced by the improvement of the markers cited above.

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In vitrokinetics of the oxidative reactivity of nitrate and nitrite in the rat erythrocyte

Cited by 14 publications

References 8 publications

Sodium nitrite enhances generation of reactive oxygen species that decrease antioxidant power and inhibit plasma membrane redox system of human erythrocytes

Sodium nitrite enhances generation of reactive oxygen species that decrease antioxidant power and inhibit plasma membrane redox system of human erythrocytes

Altered Membrane Structure and Surface Potential in Homozygous Hemoglobin C Erythrocytes

Hyparrhenia hirta: A potential protective agent against hematotoxicity and genotoxicity of sodium nitrate in adult rats

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