AIM： To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes.METHODS： Ten male SD rats weighing 80N120 g were randomly divided in...AIM： To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes.METHODS： Ten male SD rats weighing 80N120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in fluoride group had free access to deionized water containing 150 mg/L sodium fluoride （NaF）. The animals in control group were given distilled water. Four weeks later, the animals were killed. Reactive oxygen species （ROS） in oral mucosa and liver were measured by Fenton reaction, lipid peroxidation product, malondialdehyde （MDA）, was detected by thiobarbituric acid （TBA） reaction, reduced glutathione （GSH） was assayed by dithionitrobenzoic acid （DTNB） reaction. DNA damage in oral mucosal cells and hepatocytes was determined by single cell gel （SCG） electrophoresis or comet assay. Apoptosis and cell cycle in oral mucosal cells and hepatocytes were detected by flow cytometry.RESULTS： The contents of ROS and MDA in oral mucosa and liver tissue of fluoride group were significantly higher than those of control group （P〈 0.01）, but the level of GSH was markedly decreased （P〈 0.01）. The contents of ROS, MDA and GSH were （134.73 ＋ 12.63） U/mg protein, （1.48 ＋ 0.13） mmol/mg protein and （76.38 ~ 6.71） mmol/ mg protein in oral mucosa respectively, and （143.45＋ 11.76） U/mg protein, （1.44：1：0.12） mmol/mg protein and （78.83±7.72） mmol/mg protein in liver tissue respectively. The DNA damage rate in fluoride group was 50.20% in oral mucosal cells and 44.80% in hepatocytes, higher than those in the control group （P 〈0.01）. The apop- tosis rate in oral mucosal cells was （13.63 ＋ 1.81） % in fluoride group, and （t2.76＋ 1.67） % in hepatocytes, higher than those in control group. Excess fluoride could differently lower the number of oral mucosal cells and hepatocytes at G0/G1 and S G2/M phases （P〈 0.05）.CONCLUSION： Excess fluoride can induce oxi展开更多
Objective To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. Methods Wistar rats were given distilled water containing sodium fluor...Objective To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. Methods Wistar rats were given distilled water containing sodium fluoride （50 mg/L NaF） and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals （four males and four females）. Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation （0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4 · 7H2O）; and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation （0.2 mg/kg Na2 SeO3 and29.6 mg/kg ZnSO4 · 7H20）. The activities of serum glutathione peroxidase （GSH-Px）, kidney superoxide dismutase （SOD）, and the levels of malondialdehyde （MDA） and glutathione （GSH） in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry. Results NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urine γ -glutarnyl transpeptidase （ γ -GT）, inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosls, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly. Conclusion Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.展开更多
文摘AIM： To study the effect of fluoride on oxidative stress, DNA damage and apoptosis as well as cell cycle of rat oral mucosal cells and hepatocytes.METHODS： Ten male SD rats weighing 80N120 g were randomly divided into control group and fluoride group, 5 animals each group. The animals in fluoride group had free access to deionized water containing 150 mg/L sodium fluoride （NaF）. The animals in control group were given distilled water. Four weeks later, the animals were killed. Reactive oxygen species （ROS） in oral mucosa and liver were measured by Fenton reaction, lipid peroxidation product, malondialdehyde （MDA）, was detected by thiobarbituric acid （TBA） reaction, reduced glutathione （GSH） was assayed by dithionitrobenzoic acid （DTNB） reaction. DNA damage in oral mucosal cells and hepatocytes was determined by single cell gel （SCG） electrophoresis or comet assay. Apoptosis and cell cycle in oral mucosal cells and hepatocytes were detected by flow cytometry.RESULTS： The contents of ROS and MDA in oral mucosa and liver tissue of fluoride group were significantly higher than those of control group （P〈 0.01）, but the level of GSH was markedly decreased （P〈 0.01）. The contents of ROS, MDA and GSH were （134.73 ＋ 12.63） U/mg protein, （1.48 ＋ 0.13） mmol/mg protein and （76.38 ~ 6.71） mmol/ mg protein in oral mucosa respectively, and （143.45＋ 11.76） U/mg protein, （1.44：1：0.12） mmol/mg protein and （78.83±7.72） mmol/mg protein in liver tissue respectively. The DNA damage rate in fluoride group was 50.20% in oral mucosal cells and 44.80% in hepatocytes, higher than those in the control group （P 〈0.01）. The apop- tosis rate in oral mucosal cells was （13.63 ＋ 1.81） % in fluoride group, and （t2.76＋ 1.67） % in hepatocytes, higher than those in control group. Excess fluoride could differently lower the number of oral mucosal cells and hepatocytes at G0/G1 and S G2/M phases （P〈 0.05）.CONCLUSION： Excess fluoride can induce oxi
文摘Objective To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. Methods Wistar rats were given distilled water containing sodium fluoride （50 mg/L NaF） and were gavaged with different doses of selenium-zinc preparation for six months. Four groups were used and each group had eight animals （four males and four females）. Group one, sham-handled control; group two, 50 mg/L NaF; group three, 50 mg/L NaF with a low dose of selenium-zinc preparation （0.1 mg/kg Na2 SeO3 and 14.8 mg/kg ZnSO4 · 7H2O）; and group four, 50 mg/L NaF with a high dose of selenium-zinc preparation （0.2 mg/kg Na2 SeO3 and29.6 mg/kg ZnSO4 · 7H20）. The activities of serum glutathione peroxidase （GSH-Px）, kidney superoxide dismutase （SOD）, and the levels of malondialdehyde （MDA） and glutathione （GSH） in the kidney were measured to assess the oxidative stress. Kidney cell apoptosis and cell cycle were detected by flow cytometry. Results NaF at the dose of 50 mg/L increased excretion of fluoride in urine, promoted activity of urine γ -glutarnyl transpeptidase （ γ -GT）, inhibited activity of serum GSH-PX and kidney SOD, reduce kidney GSH content, and increased kidney MDA. NaF at the dose of 50 mg/L also induced rat renal apoptosls, reduced the cell number of G2/M phase in cell cycle, and decreased DNA relative content significantly. Selenium and zinc inhibited effects of NaF on oxidative stress and apoptosis, promoted the cell number of G2/M phase in cell cycle, but failed to increase relative DNA content significantly. Conclusion Sodium fluoride administered at the dose of 50 mg/L for six months induced oxidative stress and apoptosis, and changes the cell cycle in rat renal cells. Selenium and zinc antagonize oxidative stress, apoptosis, and cell cycle changes induced by excess fluoride.
