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.
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.
Chem Biol Interact. 2021 Nov 1;349:109663. doi: 10.1016/j.cbi.2021.109663. Epub 2021 Sep 20.
The problem of excessive aluminum (Al) content in food is widespread. After Al enters the body, it can cause mineral metabolism imbalance and reactive oxygen species (ROS) overproduction, which ultimately leads to bone impairment. ROS is mainly produced in mitochondria and acts on mitochondria. Mitochondrial damage is closely related to mitophagy and apoptosis. In order to clarify whether ROS-mediated mitophagy and apoptosis are involved in Al-induced femoral impairment, forty-eight male C57BL/6 N mice were exposed to AlCl (179.3 mg/kg) and/or NAC (100 mg/kg) for 90 days. Our results showed that NAC inhibited the mitophagy and apoptosis, and alleviated growth inhibition, mineral metabolism imbalance, structural damage, decreased bone mineral density and decreased bone formation factor expressions in the femora of Al-treated mice. These results suggest that ROS-mediated mitophagy and apoptosis are involved in Al-induced femoral impairment in mice, exogenous ROS clearance is a potential strategy for the treatment of Al-induced bone impairment.
食品中铝（Al）含量过高的问题普遍存在。Al 进入人体后，可引起矿物质代谢失衡和活性氧（ROS）过度产生，最终导致骨损伤。ROS 主要在线粒体中产生，并作用于线粒体。线粒体损伤与自噬和细胞凋亡密切相关。为了阐明 ROS 介导的自噬和细胞凋亡是否参与 Al 诱导的股骨损伤，将 48 只雄性 C57BL/6N 小鼠暴露于 AlCl（179.3mg/kg）和/或 NAC（100mg/kg）中 90 天。结果显示，NAC 抑制了自噬和细胞凋亡，并缓解了 Al 处理小鼠的生长抑制、矿物质代谢失衡、结构损伤、骨密度降低和骨形成因子表达降低。这些结果表明，ROS 介导的自噬和细胞凋亡参与了 Al 诱导的小鼠股骨损伤，外源性 ROS 清除可能是治疗 Al 诱导的骨损伤的一种潜在策略。
