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首页> 外文期刊>Journal of applied toxicology >Nanosized carbon black exposure induces neural injury: effects on nicotinamide adenine dinucleotide phosphate oxidases and endoplasmic reticulum stress
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Nanosized carbon black exposure induces neural injury: effects on nicotinamide adenine dinucleotide phosphate oxidases and endoplasmic reticulum stress

机译：纳米碳黑色暴露诱导神经损伤：对烟酰胺腺嘌呤二核苷酸磷酸酯氧化酶和内质网胁迫的影响

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Abstract Carbon black in ambient air is believed to be the cause of many diseases; however, its potential neural toxicity and the underlying mechanisms remain poorly understood. The present study is to evaluate the toxic effects of carbon black nanoparticles, Printex 90, on the neural cell line PC12. The study revealed that Printex 90 treatment significantly decreased cell viability, accompanied by an enormous increase in reactive oxygen species generation and a decrease in ATP. Additionally, NOX2 and NOX4, 4hydroxynonenal, endoplasmic reticulum (ER) stress marker proteins (IRE1? ATF6, GRP78, PERK and the downstream target protein CHOP) and antioxidative enzymes (glutathione and superoxide dismutase) were evaluated. It showed that Printex 90 significantly upregulated 4hydroxynonenal, NOX2 and NOX4 expression, and the levels, or activity, of glutathione and superoxide dismutase, were markedly reduced. For the ER stressassociated proteins, Printex 90 induced a significant increase of IRE1? ATF6, GRP78, pPERK and CHOP expression. Collectively, these results demonstrate that NOX and ER stress are involved in Printex 90mediated neural damage. Therefore, decreased ER stress and NOXderived reactive oxygen species generation may provide compensatory protective effects and attenuate Printex 90induced neural injury.
机译：在环境空气中的抽象炭黑被认为是许多疾病的原因;然而，其潜在的神经毒性和潜在机制仍然明白很差。本研究是评估炭黑纳米颗粒，Printex 90，在神经细胞系PC12上的毒性作用。该研究表明，Printex 90治疗显着降低了细胞活力，伴随着反应性氧物种产生的巨大增加和ATP的降低。另外，评估NOx2和NOX4，4羟基壬烯，内质网（ER）应激标记蛋白（IRE1〜ATF6，GRP78，PERK和下游靶蛋白键）和抗氧化酶（谷胱甘肽和超氧化物歧化酶）。结果表明，Printex 90显着上调的4个羟基壬烯，NOx2和NOX4表达，谷胱甘肽和超氧化物歧化酶的水平或活性显着降低。对于ER胁迫性蛋白质，Printex 90诱导IS1的显着增加？ ATF6，GRP78，PPERK和CHOP表达。总的来说，这些结果表明NOx和ER压力参与了Printex 90介导的神经损伤。因此，降低的ER应激和中间的反应性氧物种产生可以提供补偿性保护作用，并衰减30次诱导的神经损伤。

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