<br>硒代蛋氨酸通过鸡脑中的 NRF2/GPX4 通路减轻十溴二苯醚诱导的氧化应激和铁死亡,Journal of Hazardous Materials

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硒代蛋氨酸通过鸡脑中的 NRF2/GPX4 通路减轻十溴二苯醚诱导的氧化应激和铁死亡
Journal of Hazardous Materials ( IF 12.2 ) Pub Date : 2023-12-22 , DOI: 10.1016/j.jhazmat.2023.133307
Bowen Dong ₁ , Yangyang Jiang ₁ , Bendong Shi ₁ , Zhuoqi Zhang ₁ , Ziwei Zhang ₂

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十溴二苯醚（BDE209）是一种有毒的环境污染物，可引起动物的神经毒性、行为异常和认知障碍。然而，BDE209 诱导的神经损伤的具体机制和有效的预防和治疗干预措施缺乏。尽管硒代蛋氨酸（Se-Met）具有显着的解毒作用并保护神经系统，但目前尚不清楚 Se-Met 是否能抵消 BDE209 的毒性作用。对于体内测试，我们将 60 只 1 周龄的 hy-line 白色品种雏鸡随机分为 Con、BDE209、Se-Met 和 BDE209 +Se-Met 组。进行了体外实验，将鸡胚脑神经元暴露于 BDE209、Se-Met、N-乙酰半胱氨酸（NAC，一种 ROS 抑制剂）和 RSL3（一种 GPX4 抑制剂）。我们证明 BDE209 诱导鸡脑氧化应激和铁死亡，主要表现为线粒体萎缩、嵴断裂、Fe2+ 和 MDA 含量增加、抗氧化酶活性降低以及抑制脑神经元中 NRF2/GPX4 信号通路。然而，Se-Met 补充剂通过激活 NRF2/GPX4 通路、减少线粒体损伤、增强抗氧化酶活性和缓解铁死亡来逆转这些变化。本研究深入了解了 BDE209 相关神经毒性的机制，并建议 Se-Met 作为预防和控制 BDE209 中毒的有效措施。

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Selenomethionine alleviates decabromodiphenyl ether-induced oxidative stress and ferroptosis via the NRF2/GPX4 pathway in the chicken brain

Decabromodiphenyl ether (BDE209) is a toxic environmental pollutant that can cause neurotoxicity, behavioral abnormalities, and cognitive impairment in animals. However, the specific mechanisms of BDE209-induced neurological injury and effective preventative and therapeutic interventions are lacking. Even though selenomethionine (Se-Met) has a significant detoxification effect and protects the nervous system, it remains unclear whether Se-Met can counteract the toxic effects of BDE209. For the in vivo test, we randomly divided 60 1-week-old hy-line white variety chicks into the Con, BDE209, Se-Met, and BDE209 +Se-Met groups. In vitro experiments were performed, exposing chick embryo brain neurons to BDE209, Se-Met, N-Acetylcysteine (NAC, a ROS inhibitor), and RSL3 (a GPX4 inhibitor). We demonstrated that BDE209 induced oxidative stress and ferroptosis in the chicken brain, which mainly manifested as mitochondrial atrophy, cristae breakage, increased Fe2+ and MDA content, decreased antioxidant enzyme activity, and the inhibition of the NRF2/GPX4 signaling pathway in the brain neurons. However, Se-Met supplementation reversed these changes by activating the NRF2/GPX4 pathway, reducing mitochondrial damage, enhancing antioxidant enzyme activity, and alleviating ferroptosis. This study provides insight into the mechanism of BDE209-related neurotoxicity and suggests Se-Met as an effective preventative and control measure against BDE209 poisoning.

更新日期：2023-12-22

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