Nickel(II)-Induced Oxidative Stress, Apoptosis, G2/M Arrest, and Genotoxicity in Normal Rat Kidney Cells

被引:51
作者
Chen, Chang-Yu [1 ]
Lin, Tsu-Kung [3 ]
Chang, Yi-Chuang [2 ]
Wang, Yi-Fen [1 ]
Shyu, Huey-Wen [1 ]
Lin, Kuan-Hua [1 ]
Chou, Miao-Chen [1 ]
机构
[1] Fooyin Univ, Dept Med Technol, Kaohsiung, Taiwan
[2] Fooyin Univ, Dept Nursing, Kaohsiung, Taiwan
[3] Chang Gung Mem Hosp, Dept Neurol, Kaohsiung, Taiwan
来源
JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES | 2010年 / 73卷 / 08期
关键词
PROTEIN CROSS-LINKS; HAMSTER OVARY CELLS; LIPID-PEROXIDATION; HYDROGEN-PEROXIDE; MAMMALIAN-CELLS; NICKEL CHLORIDE; STRAND BREAKAGE; DNA-DAMAGE; INDUCED CARCINOGENESIS; HUMAN-LYMPHOCYTES;
D O I
10.1080/15287390903421250
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
In order to elucidate the effects of nickel (Ni) on oxidative stress, apoptosis, and genotoxicity in renal cells, the levels of intracellular oxidants, lipid peroxidation, apoptotic proteins, and DNA damage were measured in normal rat kidney (NRK) cells after nickel chloride (NiCl2) treatment. NiCl2 appeared to increase the formation of the fluorescent oxidized compound (dichlorofluorescein, DCF) and levels of thiobarbituric acid-reactive substances (TBARS). In flow cytometric analysis, a rise in cell proportion in sub-G1 phase occurred in a concentration-dependent manner. After Ni treatment, there was reduced expression of Bcl-2 and Bcl-xL proteins, while induced Bad and Bax proteins expression was higher. Single-strand DNA breakage induced by Ni in NRK cells was determined by comet assay. Significant increase DNA damage score (arbitrary units) was noted in a concentration-related manner after treatment with Ni. Induction of intracellular oxidants by Ni was accompanied by an increasing frequency of DNA strand breakage. Our data indicate that Ni-induced oxidative stress and genotoxicity in NRK cells may involve reactive oxygen intermediates, and that Bcl family-mediated signaling pathway may be involved in positive regulation of Ni-induced renal cytotoxicity.
引用
收藏
页码:529 / 539
页数:11
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