Mechanisms involved in reproductive toxicity caused by nickel nanoparticle in female rats
ABSTRACT Nickel nanoparticles (Ni NPs) are associated with reproductive toxicity. However, the mechanisms of reproductive toxicity are unclear. Our goal was to explore further reproductive toxicity induced by nickel nanoparticle and mechanisms involved in this process, including the role of oxidativ...
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Published in: | Environmental toxicology Vol. 31; no. 11; pp. 1674 - 1683 |
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Main Authors: | , , , , |
Format: | Journal Article |
Language: | English |
Published: |
United States
Blackwell Publishing Ltd
01-11-2016
Wiley Subscription Services, Inc |
Subjects: | |
Online Access: | Get full text |
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Summary: | ABSTRACT
Nickel nanoparticles (Ni NPs) are associated with reproductive toxicity. However, the mechanisms of reproductive toxicity are unclear. Our goal was to explore further reproductive toxicity induced by nickel nanoparticle and mechanisms involved in this process, including the role of oxidative stress and apoptosis. According to the one‐generation reproductive toxicity standard, rats were exposed to nickel nanoparticles by gavage and we selected indicators including ultrastructural, reactive oxygen species (ROS), oxidant and antioxidant enzymes, and cell apoptosis‐related factors. Ultrastructural results of ovaries showed mitochondrion swelling, disappearance of mitochondrial cristae, and enlargement of the endoplasmic reticulum in the exposure groups. NiNPs had significantly decreased the activity of SOD and CAT, and had increased the levels of ROS, MDA, and NO in comparison with the control groups. The mRNA expressions of caspase‐3, caspase‐8, and caspase‐9 and the expressions of Fas, Cyt c, Bax, and Bid protein on the ovaries significantly increased. At the same time, the expressions of Bcl‐2 protein were significantly decreased. Based on these results, oxidative stress and cell apoptosis may play the important roles in inducing reproductive toxicity after NiNPs treatment. © 2015 Wiley Periodicals, Inc. Environ Toxicol 31: 1674–1683, 2016. |
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Bibliography: | ark:/67375/WNG-J1T6HNL4-6 ArticleID:TOX22288 istex:24E41FF58D33DACF34D0D85E9D65DCB838E95218 The authors declare no competing financial interest. ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 1520-4081 1522-7278 |
DOI: | 10.1002/tox.22288 |