Cytotoxicity and genotoxicity of CuO nanoparticles in sea urchin spermatozoa through oxidative stress

被引:77
作者
Gallo, Alessandra [1 ]
Manfra, Loredana [1 ,2 ]
Boni, Raffaele [3 ]
Rotini, Alice [4 ]
Migliore, Luciana [4 ]
Tosti, Elisabetta [1 ]
机构
[1] Stn Zool Anton Dohrn, Dept Biol & Evolut Marine Organisms, I-80121 Naples, Italy
[2] Inst Environm Protect & Res ISPRA, Rome, Italy
[3] Univ Basilicata, Dept Sci, I-75100 Potenza, Italy
[4] Univ Tor Vergata, Dept Biol, Rome, Italy
关键词
Copper oxide nanoparticles; Cytotoxicity; Genotoxicity; Oxidative stress; Sea urchin; Sperm quality; COPPER-OXIDE NANOPARTICLES; ENGINEERED NANOPARTICLES; DEVELOPMENTAL ABNORMALITIES; REPRODUCTIVE MECHANISMS; CRASSOSTREA-VIRGINICA; AQUATIC INVERTEBRATES; SILVER NANOPARTICLES; MARINE-INVERTEBRATES; SPERM MOTILITY; EASTERN OYSTER;
D O I
10.1016/j.envint.2018.05.034
中图分类号
X [环境科学、安全科学];
学科分类号
08 ; 0830 ;
摘要
Copper oxide nanoparticles (CuO NPs) are extensively used in various industrial and commercial applications. Despite their wide application may lead to the contamination of marine ecosystem, their potential environmental effects remain to be determined. Toxicity assessment studies have primarily focused on investigating the effects of CuO NPs on fertilization success and embryo development of different sea urchin species while the impact on sperm quality have never been assessed. In this line, this study aims to assess the effects of CuO NPs on the spermatozoa of the sea urchin Paracentrotus lividus. After sperm exposure to CuO NPs, biomarkers of sperm viability, cytotoxicity, oxidative stress, and genotoxicity as well as morphology were evaluated. Results showed that CuO NPs exposure decreased sperm viability, impaired mitochondrial activity and increased the production of reactive oxygen species (ROS) and lipid peroxidation. Furthermore, CuO NPs exposure caused DNA damage and morphological alterations. Together with the antioxidant rescue experiments, these results suggest that oxidative stress is the main driver of CuO NP spermiotoxic effects. The mechanism of toxicity is here proposed: the spontaneous generation of ROS induced by CuO NPs and the disruption of the mitochondrial respiratory chain lead to production of ROS that, in turn, induce lipid peroxidation and DNA damage, and result in defective spermatozoa up to induce sperm cytotoxicity. Investigating the effects of CuO NPs on sea urchin spermatozoa, this study provides valuable insights into the mechanism of reproductive toxicity induced by CuO NPs.
引用
收藏
页码:325 / 333
页数:9
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