Protective effects of quercetin against sodium fluoride-induced oxidative stress in rat erythrocytes (original) (raw)
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Food Chemistry, 2012
The protective effects of quercetin against sodium fluoride induced oxidative stress were examined in rat's liver. Rats were divided into five groups. The first group served as normal group that was treated with standard diet. The second group was intoxicated with sodium fluoride (600 ppm) through drinking water for 1 week. The third, fourth and fifth groups were treated with quercetin at a dose of 10 and 20 mg/kg and vitamin C (as the positive control) at a dose of 10 mg/kg intraperitoneally for 1 week before sodium fluoride intoxication, respectively. After 1 week, activities of superoxide dismutase and catalase, level of reduced glutathione and lipid peroxidation end product were determined in the homogenates of rat liver. The results of the present study suggested that quercetin protects rat liver from sodium fluoride induced oxidative stress, probably via its antioxidant activity.
Effect of fluoride intoxication on lipidperoxidation and antioxidant status in experimental rats
Toxicology, 2004
Fluoride is a potent enzyme poison. Thirty ground water samples from Vellore District, Tamil Nadu, India were analysed for fluoride content and it was revealed that the fluoride content of 24 samples were over and above the permissible limits. In the present study, the experimental rats were orally treated with 25 ppm of fluoride/rat/day for 8 and 16 weeks, respectively, and the levels of lipid peroxidation and antioxidant enzymes were studied to evaluate fluoride intoxication. An increase in the level of lipid peroxides along with a concomitant decrease in the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and reduced glutathione content were observed in fluoride administered groups of rats. The altered antioxidant status may be attributed to the increased generation of free radicals.
Toxicology International, 2011
This experiment was designed to investigate the extent of peroxidative changes and histological alterations in the myocardium of rats exposed to high fluoride for two generations, in addition to ameliorative role of selenium and vitamin E on the above indices. Adult albino Wistar rats were given fluoride through drinking water (200 ppm F) and maintained subsequently for two generations, while they were exposed to fluoride throughout the experiment. Fluoride treatment significantly increased the lipid peroxidation and decreased the activity of antioxidant enzymes, viz., catalase, superoxide dismutase, and glutathione level in auricle and ventricle regions of the heart. Decreased feed and water consumption, organ somatic index and marginal drop in body growth rate were observed. Decreased antioxidant enzymes and increased malondialdehyde levels might be related to oxidative damage that occurs variably in the myocardium of rats. Biochemical changes were supported by the histological observations, which also revealed that chronic exposure to fluoride causes damage to the myocardium. Results of this study can be taken as an index of cardio-toxicity in rats exposed to water fluoridation. Further, oral supplementation of selenium and vitamin E not only inhibited oxidative stress but also enhanced the activities of antioxidant enzymes. Administration of antioxidants during fluoride exposure significantly overcame cardiac fluoride toxicity and therefore may be a therapeutic strategy for fluorotic victims.
Effect of Fluoride Toxicity on Some Clinical, Bioch emical and Physiological Aspects of Albino Rats
2012
Fluorine is a necessary biological trace element for human health. However, fluoride accumulation leads to cascading effects resulting in altered physiological functions in human being. The objective of the present study was to find out the extend of oxidative damage caused by reactive oxygen species (ROS), generated by the action of fluoride that alter the activities of the enzymes involved in the defense against free radicals and substantially influence the damaging process in brain, kidney and liver. To perform the experiment, healthy albino rats were ingested with fluoride water (5, 10, 15 and 20 ppm) for 60 days for generation of ROS in their body. The data revealed that reduction of body weight and somatic index were observed after the ingestion of 10, 15 and 20 ppm of fluoride water. Higher doses of fluoride water altered the hematological parameters leading to anaemic condition. The percentage of neutrophil is significantly increased (p<0.01) in high fluoride concentration. Total count is also dramatically reduced as compared to control. The antioxidant enzymatic parameters such as Superoxide dismutase (SOD), Glutathione transferase (GST), and catalase decreased significantly (p<0.01) in brain tissues. Loss of activity of some liver enzymes (SGPT and SGOT) indicate the decreased liver activity due to generation of ROS in rat body. The serum protein, Cholesterol and phospholipids were also significantly reduced in all the treatments studied (p<0.01). Glycogen, Cholesterol and Ascorbic acid of liver and heart tissues showed diminished activities following fluoride water treatment. Thus, the present study showed that accumulation of fluoride increases free radical production inhibits the antioxidative enzymes which probably make the tissue more susceptible to biochemical injury. From the study, it can be further concluded that excess fluoride water exposure caused altered blood cells and produce toxic effects on brain, heart and liver.
Fetotoxicity of fluoride in rats and the protective action of some antioxidants
Fluoride, 2006
The aim of this study was to assess the efficacy of antioxidants to prevent or alleviate fluoride (F) toxicity in pregnant female Wistar rats and their fetuses. Groups of pregnant rats (10 in each group) were treated by oral intubation with F (40 mg F-/kg bw/day from NaF), antioxidants (a mixture of vitamins A, C, and E and selenium) (25 mg/kg bw/day), and a combination of F and antioxidants at the same dosage levels, respectively, from the 8 th to the 19 th day of gestation. A control group received tap water. No significant change occurred among treated groups in outcome of pregnancy (no. of resorbed, dead, live normal, and abnormal fetuses/ litter) on gestational day 20. However, fetuses of F-treated rats exhibited significant reduction of body weight and length concomitant with a significant decrease of total protein content in liver tissue. On the other hand, the F concentration in serum and amniotic fluid of F-treated rats was significantly higher than all other groups. Pregnant rats with higher serum F concentration had a significantly lower serum Ca level and a higher serum P concentration with a non-significant reduction of serum total protein in comparison with the control. Administration of the antioxidants reduced the F-induced changes. Less fetal growth retardation occurred in the rats treated with both F and the antioxidants than in those treated with F alone. Moreover, antioxidant treatment resulted in some recovery of serum Ca and P levels in the Ftreated group. Antioxidants were therefore found to protect against or ameliorate Finduced toxicity in pregnant rats and their fetuses.
Ameliorative Effects of Quercetin on Sodium Fluoride-Induced Oxidative Stress in Rat’s Kidney
Renal Failure, 2012
Objective: The in vivo nephroprotective effect of quercetin against sodium fluoride (NaF)-induced damage was studied. Methods: Renal injury was induced by daily administration of NaF (600 ppm) through drinking water for 1 week. The levels of reduced glutathione (GSH), lipid peroxidation as well as superoxide dismutase and catalase activity of kidney homogenates were determined. The serum markers of glomerular damage, including creatinine, serum urea, and blood urea nitrogen levels, were also assessed. Results: The study revealed that administration of fluoride resulted in a significant downregulation of antioxidant defenses coupled with an increased serum level of glomerular damage markers. The administration of quercetin prior to fluoride reversed the antioxidant-oxidant balance to control (fluoride-untreated) level. The level of protection obtained for the 20 mg/kg quercetin treatment was equivalent to the positive control, ascorbic acid (10 mg/kg). The therapeutic implication of antioxidants in fluoride-induced nephrotoxicity is discussed. Conclusions: This study showed that NaF intoxication caused renal damage by increasing oxidative stress, and quercetin and vitamin C administration gave protection against fluoride-induced oxidative stress to some degree.
Silymarin and quercetin abrogates fluoride induced oxidative stress and toxic effects in rats
Molecular & Cellular Toxicology, 2011
Flavonoids have been extensively studied and reported to possess widespread biological activities, including antioxidant and chelating properties. They have been proposed to exert beneficial effects in a multitude of diseased states generated due to oxidative stress. Therapeutic efficacy of oral administration of Silymarin and Quercetin after fluoride exposure (50 ppm in drinking water for 45 days) was investigated in rats. Animals exposed to fluoride showed a marked enhancement in reactive oxygen species (ROS), a significant decrease in reduced glutathione (GSH) in blood. In brain and kidney also, a significant elevation in ROS and Thiobarbituric Acid Substances (TBARS) level was noted accompanied by a significant decline in reduced/oxidized glutathione (GSH: GSSG) ratio. Furthermore, significant protection was observed in altered neurotransmitters level following the administration of Silymarin and Quercetin. Interestingly, both the flavonoids were able to reduce the level of fluoride from blood and kidney suggesting that the two flavonoids have the ability to bind fluoride ion too. It can be concluded from the results that, posttreatment with these flavonoids not only significantly protects against fluoride-induced oxidative stress but reduce its burden too from blood and tissues.
Acta biochimica Polonica, 2015
Quercetin, a member of the flavonoid family is a major antioxidant acquired in humans by food consumption, while Cadmium fluoride (CdF2) is one of the naturally occurring chemicals having adverse effects. The protective effect of quercetin on time dependent oxidative damage induced in mice liver by CdF2 was studied in the following groups of mice consisting of six mice each: (i) control group; (ii) mice treated with single i.p injection of 2 mg/kg bw CdF2 for 24 h; (iii) mice treated with single i.p injection of 2 mg/kg bw CdF2 for 48 h; (iv) mice treated with single i.p injection of quercetin (100 mg/kg bw); (v) mice treated with i.p injection of 100 mg/kg bw of quercetin followed by i.p injection of CdF2 (2 mg/kg bw) for 24 h; and (vi) mice treated with i.p injection of 100mg/kg bw of quercetin followed by CdF2 (2 mg/kg bw) for 48 h. Administration of quercetin two hours before CdF2 significantly reduced the biochemical alterations in reduced glutathione, ascorbic acid, lipid pero...
Fluoride and lipid peroxidation: A comparative study in different rat tissues
Bulletin of Environmental Contamination and Toxicology, 1986
The toxic effects due to fluoride are not only confined to the skeletal tissues but deleterious effects of fluoride on central nervous system, gastrointestinal tract, liver, kidneys, cardiovascular system, respiratory tract and muscles have also been reported (Zhavoronkov 1977). Alterations in the permeability of membranes and membrane bound enzymes under the influence of fluoride have been reported (Martin et al. 19gi0). Lipid peroxidation has been suspected to play an important role in wide variety of pathological and degradative conditions (Tappel 1973). Many studies suggest that the influence of various environmental pollutants (Mudd and Freeman 1977) are closely related to lipid peroxidation.
Fluoride induced oxidative stress, immune system and apoptosis in animals: a review
Halfway through the twentieth century, fluoride piqued the interest of toxicologists due to its deleterious effects due to high concentrations in animals as well as in human populations suffering from several types of disorders and in in-vivo experimental models. Until the 1990s, the toxicity of fluoride was largely ignored due to its " good reputation " for preventing caries via topical application and in dental toothpaste. However, in the last decade, interest in its undesirable effects has resurfaced due to the awareness that this element interacts with cellular systems even at low doses. In recent years, several investigations demonstrated that fluoride can induce oxidative stress and modulate intracellular redox homoeostasis; lipid peroxidation and protein carbonyl content, as well as alter gene expression and cause apoptosis. Genes modulated by fluoride include those related to the stress response, metabolic enzymes, the cell cycle, cell–cell communications and signal transduction. The primary purpose of this review is to examine recent findings on the effects of fluoride on oxidative stress, immune system and apoptosis in the animal as well as in human system.