Mechanisms of housedust-induced toxicity in primary human corneal epithelial cells: Oxidative stress, proinflammatory response and mitochondrial dysfunction

Human cornea is highly susceptible to damage by dust. Continued daily exposure to housedust has been associated with increasing risks of corneal injury, however, the underlying mechanism has not been elucidated. In this study, a composite housedust sample was tested for its cytotoxicity on primary human corneal epithelial (PHCE) cells, which were exposed to dust at 5–320   μg/100   μL for 24   h. PHCE cell viability showed a concentration-dependent toxic effect, attributing to elevated intracellular ROS. Moreover, when exposed at >   20–80   μg/100   μL, dust-induced oxidative damage was evidenced by increased malondialdehyde and 8-hydroxy-2-deoxyguanosine (1.3–2.3-fold) and decreased antioxidative capacity (1.6–3.5-fold). Alteration of mRNA expression of antioxidant enzymes ( SOD1 , CAT , HO-1 , TRXR1 , GSTM1 , GSTP1 , and GPX1 ) and pro-inflammatory mediators ( IL-1β , IL-6 , IL-8 , TNF-α , and MCP-1 ) were also observed. Furthermore, the mitochondrial transmembrane potential was dissipated from 9.2 to 82%. Our results suggested that dust-induced oxidative stress probably played a vital role in the cytotoxicity in PHCE cells, which may have contributed to dust-induced impairment of human cornea.