期刊
COMPARATIVE BIOCHEMISTRY AND PHYSIOLOGY C-TOXICOLOGY & PHARMACOLOGY
卷 259, 期 -, 页码 -出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/j.cbpc.2022.109395
关键词
Apoptosis; Cisplatin; Ionocyte; Mitochondria damage; Nephrotoxicity; Oxidative stress; Zebrafish
资金
- Ministry of Sci-ence and Technology, Taiwan [MOST 110-2313-B-003-003]
- Taipei Veterans General Hospital [V109D49-003-MY2, V110B-010]
This study demonstrates that exposure to cisplatin induces oxidative stress, mitochondrial damage, and apoptosis in ionocytes of zebrafish embryos.
Pharmaceuticals and personal care products are emerging environmental pollutants. Cisplatin, one of the most widely used platinum-based chemotherapeutic agents, has been found to contaminate aquatic environments. Using zebrafish embryos as a model, cisplatin was previously found to impair skin ionocytes and ion regulation. The purpose of this study was to further investigate how cisplatin damages ionocytes. Zebrafish embryos were exposed to cisplatin (0, 50, and 100 mu M) for 96 h (4-100 h post-fertilization) and then stained with fluorescent dyes to reveal mitochondrial activity (rhodamine123), apoptosis (acridine orange), and oxidative stress (CellROX/MitoSOX) in ionocytes of living embryos. Results showed that cisplatin exposure decreased rhodamine 123labeled ionocytes, induced oxidative stress in ionocytes, and promoted apoptosis in a concentration-dependent manner. Quantitative PCR analysis showed that mRNA levels of antioxidative genes (sod1, sod2, gpx1a, and cat) and an apoptotic gene (caps3a) were induced. In the time-course experiment at 96-98 h post-fertilization, cisplatin increased oxidative stress and apoptosis in ionocytes in a time-dependent manner. In conclusion, this study demonstrates that cisplatin exposure induces oxidative stress, mitochondrial damage, and apoptosis in ionocytes of zebrafish embryos.
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