- NaF enhances intracellular generation of ROS and RNS in human RBC.
- It increases oxidation of proteins, thiols and lipids.
- NaF inhibits antioxidant enzymes and lowers antioxidant power of RBC.
- Antioxidant 3,4-dihydroxybenzaldehyde mitigates NaF-induced oxidative damage in RBC.
Fluoride is an essential micronutrient that is needed for mineralization of bones and formation of dental enamel. It is a widely dispersed environmental pollutant and chronic exposure to it is toxic, resulting in malignancies and hematological damage in humans. Blood is a major and early target of environmental pollutants and toxicants like fluoride. Fluoride generates reactive oxygen species and free radicals which induce oxidative stress in target cells and mediate its toxic effects. The aim of this study was to determine the mitigating effect of plant antioxidant 3,4-dihydroxybenzaldehyde (DHB) on sodium fluoride (NaF) induced oxidative damage and cytotoxicity in isolated human red blood cells (RBC)
Isolated human RBC were treated with 0.5 mM NaF, in absence or presence of different concentrations of DHB (0.1–2.5 mM). Several biochemical parameters were analyzed in cell lysates and whole cells.
Treatment of RBC with NaF increased the formation of reactive oxygen and nitrogen species. It oxidized thiols, proteins and lipids and generated their peroxidative products. Methemoglobin level, heme degradation and lipid peroxidation were increased but cellular antioxidant status declined significantly in NaF alone treated RBC, compared to the control. NaF inhibited antioxidant, membrane bound and glycolytic enzymes in RBC. However, prior incubation of RBC with DHB significantly attenuated the NaF-induced alterations in all these parameters in a DHB concentration-dependent manner.
These results show that DHB mitigates NaF-induced oxidative damage in human RBC, probably because of its antioxidant character.
*Original abstract online at https://www.sciencedirect.com/science/article/pii/S0946672X21001784
Rutin potentially attenuates fluoride induced oxidative stress mediated cardiotoxicity, blood toxicity and dyslipidemia in rats
The present study was undertaken to evaluate cardio protective effect of rutin against sodium fluoride-induced oxidative stress mediated cardio toxicity and blood toxicity. Cardiac injury was induced by daily administration of sodium fluoride 600ppm in distilled water for 4 weeks. The animals exposed to NaF exhibited a significant increase in
Long-term exposure to low level of fluoride induces apoptosis via p53 pathway in lymphocytes of aluminum smelter workers.
Long-term occupational exposure to low level of fluoride can induce oxidative stress and apoptosis in many cells, including lymphocyte. However, the underlying mechanism remains unclear. Hence, this study was designed to explore the potential oxidative stress and apoptosis of long-term occupational exposure to low level of fluoride in aluminum smelter
Oxidative stress in children with endemic skeletal fluorosis
In the village of Kheru Nayak Thanda in the Gulbarga district of Karnataka, India, 18 children aged 3 to 10 years with endemic skeletal fluorosis were shown to have oxidative stress as evidenced by elevated levels of malondialdehyde in their red blood cells, indicating increased lipid peroxidation. Significant alterations of
Cytoprotective effects of curcumin on sodium fluoride-induced intoxication in rat erythrocytes
Curcumin is well known for its potent antioxidant activity. The result of numerous studies showed that antioxidants can protect against fluoride-induced toxicity. In the present study, protective effects of curcumin against sodium fluoride-induced toxicity in rat erythrocytes were evaluated. Curcumin (10 and 20 mg/kg) and vitamin C (10 mg/kg) were
Antioxidant defense systems in red blood cell lysates of men with dental fluorosis living in Tamil Nadu, India
The status of lipid peroxidation (LPO) and antioxidants was studied in red cell blood lysates of male subjects, aged 41-50, living in an endemic fluorosis area, Vellore district, Tamil Nadu, India. The men were divided into four groups: 1) normal healthy individuals (n=10); 2) individuals with mild dental fluorosis (n=13);
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