Arab-Nozari M, Zamani E, Latifi A, Shaki F
Bratisl Lek Listy. 2019;120(7):516-522. doi: 10.4149/BLL_2019_083.
The aim of this study was to evaluate the toxic effect of AlNPs on rat brain mitochondria and compare it with that of aluminium's ionic form.
Mitochondria were isolated from rat brain. Isolated mitochondria were treated with normal saline (Control) and different concentrations of aluminium ions (AlIs) and AlNPs (50, 100 and 200 μM). Then, the effect of AlNPs on electron transport chain complexes as well as various endpoints such as mitochondrial oxidative damage (reactive oxygen species, lipid peroxidation, glutathione, and protein carbonyl) and mitochondrial function were assessed. Also, apoptosis was evaluated by cytochrome c release, mitochondrial membrane potential and swelling.
When compared to the control group, the exposure to AlNPs showed a marked elevation in oxidative stress markers and inhibition of complex III which was accompanied by disturbance in mitochondrial function. Also, AlNPs induced a significant collapse of mitochondrial membrane potential, mitochondrial swelling, and cytochrome c release.
The comparison of mitochondrial toxicity markers between both forms of aluminium revealed that the toxic effect of AlNPs on isolated brain mitochondria was substantially greater than that that caused by AlIs, which can probably be ascribed to its higher reactivity (Tab. 1, Fig. 8, Ref. 45).
本研究旨在评估氧化铝纳米颗粒（AlNPs）对大鼠脑线粒体的毒性作用，并将其与铝离子形式的毒性作用进行比较。
从大鼠脑中分离出线粒体。将分离出的线粒体用生理盐水（对照）以及不同浓度的铝离子（AlIs）和AlNPs（50、100和200μM）进行处理。然后，评估AlNPs对电子传递链复合物以及各种终点指标的影响，如线粒体氧化损伤（活性氧、脂质过氧化、谷胱甘肽和蛋白质羰基）和线粒体功能。此外，通过细胞色素c释放、线粒体膜电位和肿胀来评估细胞凋亡。
与对照组相比，暴露于AlNPs显示氧化应激标志物显著升高，复合物III受到抑制，同时伴有线粒体功能紊乱。此外，AlNPs诱导线粒体膜电位显著崩溃、线粒体肿胀和细胞色素c释放。
两种形式铝的线粒体毒性标志物比较显示，AlNPs对分离的脑线粒体的毒性作用明显大于AlIs所造成的毒性作用，这可能归因于其更高的反应活性（表1，图8，参考文献45）。
