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Studies on the Influence of Selenium and Vitamin C on Oxidative Stress, DNA Damage and Bcl-2 Protein Expression Induced by High Fluoride

Author: WangGuiQin
Tutor: ZhaoXinHua
School: Guangdong College of Pharmacy
Course: Epidemiology and Health Statistics
Keywords: Selenium Vitamin C Fluorine Oxidative stress DNA damage Bcl-2
CLC: R599
Type: Master's thesis
Year: 2011
Downloads: 63
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Abstract


Purpose of endemic fluorosis is widely distributed in the world the endemic, China is one of the countries most affected by the epidemic. Selenium and vitamin C combined with the study of toxic effects caused by fluoride has not been reported yet. From selenium and vitamin C alone on the basis of research by investigating the effect of selenium and vitamin C the high fluoride-induced oxidative stress, DNA damage and protein expression of Bcl-2, for the next selenium and vitamin C associated caused by fluoride toxicity studies provide the basis. Methods Healthy rats were randomly divided into control group, high fluoride group, low selenium group, Se, Se, low vitamin C group, the vitamin C group and the high vitamin C group. In addition to the blank control group drinking tap water and distilled water orally, the other rats drinking 150mg/ml sodium fluoride (NaF) solution and treated by corresponding doses of sodium selenite (low selenium group: selenium acid in 4ug/ml Asia solution of sodium; in the selenium group: 8ug/ml sodium selenite; selenium group: 16ug/ml sodium selenite) or vitamin C solution (low vitamin C group: the 0.01g/ml vitamin C solution; vitamin Group C: the 0.02g/ml vitamin C solution; high vitamin C group: 0.04g/ml vitamin C solution). The administration volume are weight 5ml/kg, day 1, administration time of month. Administered one month after the rats were sacrificed to collect specimens be handled as follows: (1) the use of ion-selective electrode selection method the determination of the concentration of fluoride ions in the urine of rats; coefficient of determination of liver, kidney; 2. Determination of rat liver and kidney oxidative stress related indicators: determination of malondialdehyde (MDA), thiobarbituric acid (TBA) colorimetric method; using dithiobis nitrobenzoic acid (DTNB) method for the determination of glutathione peroxidase (GSH-Px) activity; pyrogallol autoxidation Determination of superoxide dismutase (SOD) activity. Single cell gel electrophoresis method determination of rat liver and kidney cell DNA damage. 4 by immunohistochemistry was observed in liver and kidney of the Bcl-2 protein expression levels. Results urine fluoride and organ coefficient test results: drinking sodium fluoride solution in each group after urinary fluoride concentrations were increased, the blank control group and the high fluoride group difference was statistically significant (P lt; 0.05), prompted drinking sodium fluoride solution to promote the excretion of urine fluoride. In the selenium group, the difference between low vitamin C group and the vitamin C group and the control group was statistically significant (P lt; 0.05), with high fluoride groups was no significant difference (P gt; 0.05), prompt selenium dose and low-dose vitamin C can not be improved drinking sodium fluoride causes urinary fluoride concentration increased, the low selenium group and the high fluoride group difference was statistically significant (P lt; 0.05), and with the control group was not statistically significant (P lt; 0.05). Organ coefficient between the groups was no significant difference (P gt; 0.05) Liver and kidney tissue oxidative stress-related parameters were measured results show that: Compared with the control group and the high fluoride group, the selenium group and vitamin C group liver GSH-Px were increased, and there is a statistically significant (P lt; 0.05). The liver MDA differences among the groups was not statistically significant (P gt; 0.05). Compared with the blank control group, group and high fluoride group, the low selenium group was significantly higher in liver SOD was statistically significant (P lt; 0.05). High fluoride renal GSH-Px significantly increased compared with the control group, and was statistically significant (P lt; 0.05). Low vitamin C group and the high fluoride group difference was statistically significant (P lt; 0.05) Low selenium group and renal MDA in the selenium group and blank control group difference was statistically significant (P lt; 0.05), the high selenium group and low vitamin C group and high fluoride group difference was statistically significant (P lt; 0.05) . 3.DNA damage measurement results show: liver tissue high fluoride group compared with the control group increased rate of cell damage and the difference was statistically significant (P lt; 0.05). Low selenium group, the high selenium group with high fluoride injury rate difference was statistically significant (P lt; 0.05) Differences in injury rates in the selenium group and control group was statistically significant, with high fluoride group, no significant difference (P lt; 0.05). High vitamin C group, the vitamin C group with high fluoride group was no significant difference in the rates of DNA damage (P gt; 0.05) Renal tissue of the control group was no significant difference in the injury rate of the high fluoride group (P gt; 0.05) The selenium dose group injury rate with high fluoride group injury rate was no significant difference (P gt; 0.05) Vitamin C dose group and high fluoride group cell injury rate difference was statistically significant (P lt; 0.05) 4.Bcl-2 protein expression measurement results: among the groups, liver and kidney tissue of Bcl-2 expression is not obvious, the average optical density was no significant difference (P GT; 0.05). High fluoride group and the control group compared to the average optical density value has declined but not statistically significant. For liver tissue, with increasing dose of selenium and vitamin C, the average optical density gradually increased, but no significant difference (P gt; 0.05) Conclusion 1. Rats high doses of fluoride intake, urinary fluoride concentrations were significantly increased, indicating that the fluoride experiment was a success. Low doses of selenium can improve urinary fluoride concentration increases caused due to drinking sodium fluoride, has a protective effect on the fluoride-induced renal damage. Rats after high doses of fluoride, liver tissue lipid peroxidation is not obvious, indicating that the liver fluoride-induced peroxidation certain compensatory ability. Rats after high doses of fluoride, liver cells a significant DNA damage. DNA damage induced by fluoride in the liver cells, the low-dose and high-dose selenium played antagonism. Each dose of vitamin C and sodium fluoride combined with renal cell toxicity experimental results, the mechanism needs further study. Presumably with a test dose and test time. 4 rat high doses of fluoride, the liver and kidney Bcl-2 protein expression, despite the lower but the difference was no statistically significant, suggesting that the experimental conditions, sodium fluoride is not yet on the liver and kidney Bcl-2 protein expression inhibition .

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