Abstract
Aluminium (Al) accumulates in the spleen and causes spleen apoptosis. Mitochondrial dyshomeostasis represents primary mechanisms of spleen apoptosis induced by Al. Apoptosis-inducing factor (AIF) is located in the gap of the mitochondrial membrane and can be released into the nucleus, leading to apoptosis. Phosphatase and tensin homolog (PTEN)-induced putative kinase1 (PINK1)/E3 ubiquitin ligase PARK2 (Parkin)-mediated mitophagy maintains mitochondrial homeostasis by removing damaged mitochondria, but its function in AIF-mediated spleen apoptosis induced by Al is not clear. In our study, aluminium trichloride (AlCl3) was diluted in water for 90d and administered to 75 male C57BL/6N mice at 0, 44.8, 59.8, 89.7, and 179.3mg/kg body weight. AlCl3 triggered PINK1/Parkin pathway-mediated mitophagy, induced AIF release and AIF-mediated spleen apoptosis. AlCl3 was administered to sixty male C57BL/6N mice of wild type and Parkin knockout for 90d at 0 and 179.3mg/kg body weight. The results indicated that Parkin deficiency decreased mitophagy, aggravated mitochondrial damage, AIF release and AIF-mediated spleen apoptosis induced by AlCl3. According to our results, PINK1/Parkin-mediated mitophagy and AIF-mediated spleen apoptosis are caused by AlCl3, whereas mitophagy is protective in AIF-mediated apoptosis induced by AlCl3.
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Schedule a callMore From: Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
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