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mtROS 介导线粒体自噬参与黄曲霉毒素 B 诱导的鸭肝损伤。

mtROS-mediated mitophagy is involved in aflatoxin-B induced liver injury in ducks.

机构信息

College of Animal Science and Technology, Inner Mongolia Minzu University, Tongliao 028000, China.

Key Laboratory of the Provincial Education, Department of Heilongjiang for Common Animal Disease Prevention and Treatment, College of Veterinary Medicine, Northeast Agricultural University, Harbin 150030, China.

出版信息

Comp Biochem Physiol C Toxicol Pharmacol. 2024 Sep;283:109942. doi: 10.1016/j.cbpc.2024.109942. Epub 2024 May 27.

DOI:10.1016/j.cbpc.2024.109942
PMID:38810896
Abstract

Aflatoxin B (AFB) is highly toxic to the liver and can cause excessive production of mitochondrial reactive oxygen species (mtROS) in hepatocytes, leading to oxidative stress, inflammation, fibrosis, cirrhosis, and even liver cancer. The overproduction of mtROS can induce mitophagy, but whether mtROS and mitophagy are involved in the liver injury induced by AFB in ducks remains unclear. In this study, we first demonstrated that overproduction of mtROS and mitophagy occurred during liver injury induced by AFB exposure in ducks. Then, by inhibiting mtROS and mitophagy, we found that the damage caused by AFB in ducks was significantly alleviated, and the overproduction of mtROS induced by AFB exposure could mediate the occurrence of mitophagy. These results suggested that mtROS-mediated mitophagy is involved in AFB-induced duck liver injury, and they may be the prevention and treatment targets of AFB hepatotoxicity.

摘要

黄曲霉毒素 B(AFB)对肝脏具有高度毒性,可导致肝细胞中线粒体活性氧(mtROS)过度产生,引发氧化应激、炎症、纤维化、肝硬化,甚至肝癌。mtROS 的过度产生会诱导自噬,但 mtROS 和自噬是否参与 AFB 诱导的鸭肝脏损伤尚不清楚。在本研究中,我们首先证明了在 AFB 暴露诱导的鸭肝脏损伤过程中,mtROS 和自噬过度产生。然后,通过抑制 mtROS 和自噬,我们发现 AFB 对鸭造成的损伤明显减轻,AFB 暴露引起的 mtROS 过度产生可以介导自噬的发生。这些结果表明,mtROS 介导的自噬参与了 AFB 诱导的鸭肝脏损伤,它们可能是 AFB 肝毒性的预防和治疗靶点。

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