硒锌对大鼠肾脏氧化应激、细胞凋亡和增殖周期的影响

The Role of Selenium and Zinc in Rat Renal Oxidative Stress, Apoptosis and Proliferation

将亚硒酸钠和硫酸锌配伍制备低剂量 (0 .1mg/ kg体重 Na2 Se O3 和 14.8mg/ kg体重 Zn SO4· 7H2 O)和高剂量 (0 .2 mg/ kg体重 Na2 Se O3 和 2 9.6 mg/ kg体重 Zn SO4· 7H2 O)硒锌制剂 ,通过灌胃方式给予 Wistar大鼠 ,6个月后用 TUNEL 法和流式细胞术检测大鼠肾脏细胞凋亡和细胞增殖周期的变化。结果表明 ,低剂量和高剂量硒锌均能明显诱导大鼠肾脏细胞凋亡 ,低剂量硒锌对细胞增殖周期不产生明显影响 ,而高剂量硒锌使 G2 / M期细胞减少 ,DNA相对含量下降。研究提示 :一定剂量硒锌能有限改善机体抗氧化能力 ,但仍可诱导肾脏细胞凋亡并影响 DNA合成 ,使细胞滞留于 S期 。

Wistar rats were administered through gavage with low dose (0.1 mg/kg body weight every day of sodium selenite and 14.8 mg/kg body weight every day of zinc sulfate) and high dose (0.2 mg/kg body weight every day of sodium selenite and 29.6 mg/kg body weight every day of zinc sulfate) of selenium-zinc preparation (Se-Zn) for 6 months. Renal apoptosis and proliferation in the rats were detected by using TdT-mediated dUTP nick end labeling (TUNEL) and flow cytometry. The results showed the renal apoptosis in the rats could be induced obviously by low and high doses of Se-Zn preparation. Low dose of Se-Zn preparation had no significant influence on the renal proliferation, while high dose of Se-Zn preparation could significantly reduce the cells of G 2/M period in cell cycle and lower the DNA relative content. It was suggested that certain doses of Se-Zn could improve the state of oxidative stress, induce apoptosis, alter cell cycle and interfere with DNA synthesis of rat kidney.