Levels of oxidative stress in brain and serum of rats with chronic fluorosis and antagonistic effects of Vitamin E

Abstract

Objective To detect the levels of oxidative stress in brain and serum of rats with chronic fluorosis and the antagonistic effects of vitamin E (VitE), and to reveal the role of oxidative stress in brain injury. Methods Thirty healthy SD rats were divided into three groups based on body weight by means of a random number table (10 rats in each group, half male and half female). In the control group, the rats were fed with drinking water containing less than 0.5 mg/L fluoride; in the fluoride group, the rats were fed with high doses of sodium fluoride in drinking water (50.0 mg/L) and the VitE antagonistic group were fed with the same content of fluoride in drinking water as the fluoride group, but adding VitE (50.0 mg/kg) by intragastric administration once a day. All rats were fed with normal diet (6.2 mg/kg). After exposure to fluoride for 10 months, all rats were put to death, dental fluorosis of the rats was examined and the fluoride content in bone was determined by fluoride-ion selective electrode; the activity of superoxide dismutase (SOD) was determined by the xanthine oxidase method and glutathione peroxidase (GSH-Px) by the colorimetric method, the level of malonaldehyde (MDA) by the glucosinolates barbituric acid fluorescence method and the levels of OH-, H2O2 and in rat serum and/or brain were detected by the colorimetric method. Results In the rats of the fluoride group, fluoride content in bone was higher as compared to control [bone fluoride: (211.07 ± 48.52) vs. (33.40 ± 9.26) mg/kg,P < 0.01]. The activities of SOD and GSH-Px in rat brains of the fluoride group [(20.10 ± 1.98) kU/g, (28.70 ± 19.35) kU/L] were significantly lower than those of controls [(37.05 ± 3.13) kU/g, (59.63 ± 12.83) kU/L, all P < 0.01], the activity of SOD in VitE antagonistic group [(26.27 ± 1.74) kU/g] was higher than the fluoride group (P < 0.01); the activities of SOD and GSH-Px in rat serum of the fluoride group were significantly decreased [(11.55 ± 1.75) kU/L, (79.50 ± 19.18) U/L] than those of controls [(20.79 ± 2.43) kU/L, (170.00 ± 14.68) U/L, all P < 0.01], the activity of SOD in VitE antagonistic group[(17.23 ± 0.68) kU/L] was higher than the fluoride group (P < 0.01). The levels of MDA in rat brain and serum of the fluoride group [(8.84 ± 0.69) μmol/L, (1.46 ± 0.11) nmol/L] were significantly higher than those of controls [(1.27 ± 0.74) μmol/L, (0.83 ± 0.10) nmol/L, all P < 0.01], VitE antagonistic groups [(4.51 ± 1.13) μmol/L, (1.29 ± 0.02) nmol/L] were lower than the fluoride groups (all P < 0.01). The levels of OH-, H2O2 and in rat brains of the fluoride group [(24.24 ± 1.80) kU/g, (15.28 ± 2.97) mmol/L, (6.53 ± 0.96) U/g] were significantly higher than those of controls [(11.44 ± 1.63)kU/g, (5.28 ± 1.20) mmol/L, (2.93 ± 0.42) U/g, all P < 0.01], VitE antagonistic groups [(14.43 ± 0.76) kU/g, (8.09 ± 0.55) mmol/L, (4.41 ± 0.49) U/g] were lower than the fluoride groups (all P< 0.01). Conclusions Elevated levels of oxidative stress are found in brain and serum of the rats with chronic fluorosis, which may be a main mechanism of brain injury. VitE may play an important antagonistic role in oxidative damage induced by fluoride toxicity. Key words: Fluorosis; Oxidative stress; Brain; Serum; Vitamin E