Sodium fluoride activates ERK and JNK via induction of oxidative stress to promote apoptosis and impairs ovarian function in rats

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• 作者：Yanqing Geng¹ ; ^{aqing000@163.com" class="auth_mail} ; Yiwen Qiu¹ ; ^{496597283@qq.com" class="auth_mail} ; Xueqing Liu ^{a68733172@online.cq.cn" class="auth_mail} ; Xuemei Chen ^{shirly-cxm@163.com" class="auth_mail} ; Yubin Ding ^{dingyb@gmail.com" class="auth_mail} ; Shangjing Liu ^{Liushangjing123@126.com" class="auth_mail} ; Yi Zhao ^{xiaobaozi1225@gmail.com" class="auth_mail} ; Rufei Gao ^{gao_ru_fei@163.com" class="auth_mail} ; Yingxiong Wang ^{wyx61221@aliyun.com" class="auth_mail} ; Junlin He ; ^{hejunlin_11@aliyun.com" class="auth_mail}
• 关键词：Sodium fluoride ; Female reproduction ; Ovarian apoptosis ; Oxidative stress
• 刊名：Journal of Hazardous Materials
• 出版年：15 May, 2014
• 年：2014
• 卷：272
• 期：Complete
• 页码：75-82
• 全文大小：2721 K

文摘

The toxicity of sodium fluoride (NaF) to female fertility is currently recognized; however, the mechanisms are unclear. Previously, we reported a reduction in successful pregnancy rates, ovarian atrophy and dysfunction following exposure to NaF. The purpose of this study was to elucidate the underlying molecular mechanisms. Female Sprague-Dawley rats (10 rats/group) received 100 or 200 mg/L NaF in their drinking water for 6 months or were assigned to an untreated control group. Apoptotic indices and oxidative stress indicators in blood and ovarian tissue were analyzed following sacrifice. The results confirmed the NaF-induced ovarian apoptosis, with concomitant activation of oxidative stress. Further investigations in ovarian granular cells showed that exposure to NaF activated extracellular regulated protein kinase (ERK) and c-Jun NH₂ kinase (JNK), disrupting the ERK and JNK signaling pathways, while p38 and PI3K remained unchanged. These data demonstrated that oxidative stress may play a key role in NaF-induced ovarian dysfunction by activating the apoptotic ERK and JNK signaling pathways.