Mitigating role of quercetin against sodium fluoride-induced oxidative stress in the rat brain

CONTEXT: Quercetin is a well known aglycone flavonoid that is widely found in different food sources. OBJECTIVE: In this study, the in vivo neuroprotective potential of quercetin against sodium fluoride-induced oxidative stress was evaluated. MATERIALS AND METHODS: Wistar rats were divided into five treatment groups and then subjected to daily intraperitoneally treatment with quercetin (at 10 and 20 mg/kg body weight), vitamin C (at 10 mg/kg), or vehicle. After a 1 week treatment period, all groups except saline treated (normal group), were intoxicated with sodium fluoride (NaF) for 1 week. Rat brains were then removed and homogenized for measurement of antioxidant markers including superoxide dismutase (SOD), reduced glutathione, catalase, and lipid peroxidation final products. RESULTS: The thiobarbituric acid reactive substances (TBARS) levels in the heart homogenate of sodium fluoride treated rats (42.04 ± 2.14 nmol MDA eq/g tissue) increased compared to the normal rats (35.99 ± 1.08 nmol MDA eq/g tissue). Animals which were pretreated with quercetin at 20 mg/kg for 1 week prior to sodium fluoride intoxication showed significant reduction in the TBARS level (36.13 ± 1.12 nmol MDA eq/g tissue). Also, pretreatment with quercetin (20 mg/kg) restored the SOD and catalase activities and modified the level of reduced glutathione compared with the control group (p > 0.05). DISCUSSION AND CONCLUSION: The present study revealed a potent neuroprotective potential of quercetin against NaF-induced toxicity

PROTECTIVE EFFECTS OF VITAMINS C AND E AGAINST ENDOMETRIAL DAMAGE AND OXIDATIVE STRESS IN FLUORIDE INTOXICATION

1. Fluoride (F) is an essential trace element that has protective effects against bone mineral loss. However, it becomes toxic at higher doses and induces some adverse effects on a number of physiological functions, including reproduction. The aims of this study were to examine F-induced oxidative stress that promotes production of reactive oxygen species (ROS) and to investigate the role of vitamins C and E against possible F-induced endometrial impairment in rats. 2. Rats were divided into three groups: control, F and F plus vitamins. The F group was given 100 mg/L orally for 60 days. Combined vitamins were also administered orally. Fluoride administration to control rats significantly increased endometrial malondialdehyde (MDA) but decreased superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) activities. Endometrial glandular and stromal apoptosis were investigated by DNA nick end-labelling (TUNEL) method on each sample and the mean endometrial apoptotic index (AI) was calculated. 3. Vitamin administration with F treatment caused endometrial MDA to decrease, but SOD, GSH-Px and CAT activities to increase, all to significant levels. Vitamins showed a histopathological protection against F-induced endometrial damage. There was a significant difference in the AI between the groups. Lymphocyte and eosinophil infiltration in stroma in F-treated rats were more than those in the control and F + Vit groups. 4. It can be concluded that oxidative endometrial damage plays an important role in F-induced endometrial toxicity, and the modulation of oxidative stress with vitamins reduces F-induced endometrial damage both at the biochemical and histological levels