The cross-linking between DNA damage, oxidative stress and epidermal barrier in keratinocytes after exposure to particulate matters and carbon black.

Abstract

As the largest organ, the skin provides the first line of defence against environmental pollutants. Different pollutants have varied damage to the skin due to their own physical-chemical properties. A previous epidemiological study by our team revealed that eczema was positively correlated with different air pollutants. However, the mechanism of action from different pollutants on the skin is less known. In this work, the differences among the genotoxicity, intracellular reactive oxygen species, and barrier-related parameters caused by two kinds of air pollutants, that is, S1650b and carbon black (CB) were investigated by Western blot, TUNEL, comet assay and RNA-sequences. The results indicated that both S1650b and CB caused DNA damage of keratinocytes. With the content of lipophilic polycyclic aromatic hydrocarbons (PAH), S1650b leaked into the keratinocytes easily, which activated the aromatic hydrocarbon receptor (AhR) in keratinocytes, leading to worse damage to barrier-related proteins than CB. And CB-induced higher intracellular ROS than S1650b due to the smaller size which make it enter the keratinocytes easier. RNA-sequencing results revealed that S1650b and CB both caused DNA damage of keratinocytes, and the intervention of S1650b significantly upregulated AhR, cytochrome oxidase A1 and B1 (CYP1A1 and CYP1B1) genes, while the results showed oppositely after CB intervention. The mechanism of keratinocyte damage caused by different air particle pollutants in this study will help to expand our understanding on the air pollutant-associated skin disease at cell levels.