Literature DB >> 22287616

Effects of low-dose, long-term formaldehyde exposure on the structure and functions of the ovary in rats.

Hai-xu Wang1, Xiao-yan Wang, Dang-xia Zhou, Lie-rui Zheng, Jing Zhang, Yong-wei Huo, Hong Tian.   

Abstract

Formaldehyde (FA) is a ubiquitous environmental pollutant. However, the effects of FA exposure on reproduction are still a matter of scientific controversy. In this study, we assessed the ovarian toxicity of long-term, low-dose FA exposure in rats and explored the potential oxidative stress mechanisms. A total of 30 Sprague-Dawley female rats were randomly allotted to three groups, in which rats were exposed to FA at a dose of 0 mg/m(3) (control), 0.5 mg/m(3) and 2.46 mg/m(3), respectively, by inhalation consecutively for 60 days. The results showed that the ovarian toxicity of FA is dose dependent. Ovarian structure and function in the group of rats exposed to 0.5 mg/m(3) FA showed no obvious difference when compared with those in the control group. However, the activity of superoxide dismutase was significantly decreased, whereas the level of malondialdehyde was significantly increased in ovaries of rats exposed to 2.46 mg/m(3) FA. Moreover, histopathological results demonstrated that the number and size of mature follicles significantly decreased, vascular congestion and interstitial edema in the ovaries of rats exposed to 2.46 mg/m(3) FA. In conclusion, this study may suggest that the FA level of 0.5 mg/m(3) can be considered as a safe level for FA exposure, but long-term FA exposure at a dose of 2.46 mg/m(3) has a harmful effect on ovary by inducing oxidative stress.

Entities:  

Keywords:  Formaldehyde; ovary; oxidative stress; rat; reproduction toxicity

Mesh:

Substances:

Year:  2012        PMID: 22287616     DOI: 10.1177/0748233711430983

Source DB:  PubMed          Journal:  Toxicol Ind Health        ISSN: 0748-2337            Impact factor:   2.273


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5.  miR-153-3p Targets βII Spectrin to Regulate Formaldehyde-Induced Cardiomyocyte Apoptosis.

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Review 6.  Environmental exposures associated with elevated risk for autism spectrum disorder may augment the burden of deleterious de novo mutations among probands.

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  6 in total

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