Patients who work with or near diesel fuel may have yet another hazard to look out for: damage to their eyes. According to a new study published in Experimental Eye Research, even short-term exposure triggers oxidative stress markers and inflammatory mediators in human conjunctival epithelial cells.
Researchers in Buenos Aires evaluated the effects of diesel exhaust particle (DEP) exposure after one, three and 24 hours, and measured everything from reactive oxygen species (ROS) production and lipid and protein oxidation to Nrf2 pathway activation, enzymatic antioxidants, glutathione (GSH) levels and synthesis, and cytokine release and cell proliferation.
They found DEP exposure led to an increase in ROS at each of the three time points. The cells also underwent a proinflammatory response mediated by IL-6 with longer exposure. To compensate, the cells activated Nrf2 to increase their antioxidant capacity. After 24 hours of DEP exposure, GSH levels fell as lipid-peroxidation and protein oxidation increased.
Ultimately, DEP caused hyperplasia in human conjunctival epithelial cells after one and three hours of exposure, but after that, the compensatory factors could not keep up, leading to a decrease in cell proliferation after longer exposure.
“Although after 24 hours Nrf2 pathway is still enhanced, the epithelial cell capacity to maintain redox balance is exceeded,” the researchers note. “The antioxidant enzymes activation and the depleted GSH pool are not capable of counteracting the increased ROS production, leading to oxidative damage.”
|Lasagni Vitar RM, Tau J, Janezic NS, et al. Diesel exhaust particles (DEP) induce an early redox imbalance followed by an IL-6 mediated inflammatory response on human conjunctival epithelial cells. Exp Eye Res. 2018 Jun;171:37-47.|