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.
J Agric Food Chem. 2021 Jun 2;69(21):6054-6063. doi: 10.1021/acs.jafc.1c01921. Epub 2021 May 21.
The pollution of aluminum (Al) in agricultural production and its wide application in food processing greatly increase the chance of human and animal exposure. Al can accumulate in bone and cause bone diseases by inducing oxidative stress. Mitophagy can maintain normal cell function by degrading damaged mitochondria and scavenging reactive oxygen species. However, the role of mitophagy in the bone impairment caused by Al is unknown. In this study, we demonstrated that PTEN induced putative kinase 1 (PINK1)/ E3 ubiquitin ligase PARK2 (Parkin)-mediated mitophagy was activated in the bone impairment caused by Al . Then, the Al-induced mitophagy in Parkin-deficient mice and MC3T3-E1 cells were decreased. Meanwhile, Parkin deficiency exacerbated the bone impairment, mitochondrial damage, and oxidative stress under Al exposure, both and . In general, the results reveal that Al exposure can activate PINK1/Parkin-mediated mitophagy, and the PINK1/Parkin-mediated mitophagy plays a protective role in the bone impairment caused by Al.
铝（Al）在农业生产中的污染及其在食品加工中的广泛应用大大增加了人类和动物暴露的机会。铝可以通过诱导氧化应激在骨骼中积累，从而导致骨骼疾病。自噬可以通过降解受损的线粒体和清除活性氧来维持正常的细胞功能。然而，自噬在铝引起的骨骼损伤中的作用尚不清楚。在这项研究中，我们证明了 PTEN 诱导的假定激酶 1（PINK1）/E3 泛素连接酶 PARK2（Parkin）介导的自噬在铝引起的骨骼损伤中被激活。然后，在 Parkin 缺陷型小鼠和 MC3T3-E1 细胞中，铝诱导的自噬减少。同时，Parkin 缺陷加剧了铝暴露下的骨骼损伤、线粒体损伤和氧化应激，both 和. 综上所述，这些结果表明铝暴露可以激活 PINK1/Parkin 介导的自噬，而 PINK1/Parkin 介导的自噬在铝引起的骨骼损伤中发挥保护作用。
