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Numerous studies have linked particulate matter2.5 (PM 2.5 ) to ocular surface diseases, but few studies have been conducted on the biological effect of PM 2.5  on the cornea. The objective of this study was to evaluate the harmful effect of PM2.5 on primary rat corneal epithelial cells (RCECs)  in vitro  and identify the toxic mechanism involved. Primary cultured RCECs were characterized by pan-cytokeratin (CK) staining. In PM2.5-exposed RCECs, cell viability, microarray gene expression, inflammatory cytokine levels, mitochondrial damage, DNA double-strand break, and signalling pathway were investigated. Exposure to PM 2.5  induced cytotoxicity and morphological changes in RCECs. In addition, PM 2.5  markedly up-regulated pro-inflammatory mediators but down-regulated the wound healing-related transforming growth factor-β. Furthermore, PM 2.5  promoted mitochondrial reactive oxygen species (ROS) production and mediated cellular damage to mitochondria and DNA, whereas these cellular alterations induced by PM 2.5  were markedly suppressed by a potential ROS scavenger. Noteworthy, removal of ROS selectively down-regulated the phosphorylation of p38 mitogen-activated protein kinase (MAPK) and the activation of the nuclear factor-κB (NF-κB) p65 in PM 2.5 -stimulated cells. Additionally, SB203580, a p38 MAPK inhibitor, markedly suppressed these PM 2.5 -mediated cellular dysfunctions. Taken together, our findings show that PM 2.5  can promote the ROS/p38 MAPK/NF-κB signalling pathway and lead to mitochondrial damage and DNA double-strand break, which is ultimately caused inflammation and cytotoxicity in RCECs. These findings indicate that the ROS/p38 MAPK/NF-κB signalling pathway is one mechanism involved in PM 2.5 -induced ocular surface disorders.

cutaneous and ocular toxicology

Particulate matter 2.5 promotes inflammation and cellular dysfunction  via  reactive oxygen species/p38 MAPK pathway in primary rat corneal epithelial cells