Abstract

The aim of the present study was to analyse how short wave blue and long wave red light differentially affect corneal epithelial (HCE-2) cells in culture. The corneal epithelium in situ is exposed to more blue light than in the past because of Light Emitting Diodes (LEDs) used for indoor lighting and computer, television and phone screens. Compared with cultures maintained in the dark, low intensity blue light, such as that emitted from computer screens, reduced the proliferation rate of HCE-2 cells and caused cell death at greater intensities in a dose-dependent manner. In contrast, red light at high intensity slightly enhanced the proliferation rates of HCE-2 cells and importantly blunted the negative influence of blue light on cell survival when delivered after the insult. The toxic influence of blue light on HCE-2 cells involves mitochondrial dysfunction and the activation of AIF, p38-MAPK and HO-1. Importantly, red light blocks the effects caused by blue light and enhances mitochondrial function when delivered independently. The mechanism of action of red light is to directly stimulate mitochondrial function, suggested by staining with JC-1, which results in the activation of multiple biochemical mechanisms and the ability to blunt a variety of death pathways. As a consequence, even sodium azide-induced toxicity to HCE-2 cells in culture is blunted by red light. We interpret our studies on HCE-2 cell cultures to suggest that red light can be used prophylactically to protect the corneal epithelial in situ and is also able to counteract a variety of potential environmental insults to the tissue that includes blue light. This might be of particular significance when the cornea is already affected as, for example, in dry eye.

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