Nanosized carbon black exposure induces neural injury: effects on nicotinamide adenine dinucleotide phosphate oxidases and endoplasmic reticulum stress.

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 PC-12. 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, 4-hydroxynonenal, endoplasmic reticulum (ER) stress marker proteins (IRE-1α, ATF-6, GRP78, PERK and the downstream target protein CHOP) and antioxidative enzymes (glutathione and superoxide dismutase) were evaluated. It showed that Printex 90 significantly upregulated 4-hydroxynonenal, NOX2 and NOX4 expression, and the levels, or activity, of glutathione and superoxide dismutase, were markedly reduced. For the ER stress-associated proteins, Printex 90 induced a significant increase of IRE-1α, ATF-6, GRP78, p-PERK and CHOP expression. Collectively, these results demonstrate that NOX and ER stress are involved in Printex 90-mediated neural damage. Therefore, decreased ER stress and NOX-derived reactive oxygen species generation may provide compensatory protective effects and attenuate Printex 90-induced neural injury.