Abstract
Light pollution by artificial light, might accelerate retinal diseases and circadian asynchrony. The excess of light exposure is a growing problem in societies, so studies on the consequences of long-term exposure to low levels of light are needed to determine the effects on vision. The possibility to understand the molecular mechanisms of light damage will contribute to the knowledge about visual disorders related to defects in the phototransduction. Several animal models have been used to study retinal degeneration (RD) by light; however, some important aspects remain to be established. Previously, we demonstrated that cool white treatment of 200 lux light-emitting diode (LED) induces retinal transformation with rods and cones cell death and significant changes in opsin expression in the inner nuclear layer (INL) and ganglion cell layer (GCL). Therefore, to further develop describing the molecular pathways of RD, we have examined here the oxidative stress and the fatty acid composition in rat retinas maintained at constant light. We demonstrated the existence of oxidative reactions after 5 days in outer nuclear layer (ONL), corresponding to classical photoreceptors; catalase (CAT) enzyme activity did not show significant differences in all times studied and the fatty acid study showed that docosahexaenoic acid decreased after 4 days. Remarkably, the docosahexaenoic acid diminution showed a correlation with the rise in stearic acid indicating a possible association between them. We assumed that the reduction in docosahexaenoic acid may be affected by the oxidative stress in photoreceptors outer segment which in turn affects the stearic acid composition with consequences in the membrane properties. All these miss-regulation affects the photoreceptor survival through unknown mechanisms involved. We consider that oxidative stress might be one of the pathways implicated in RD promoted by light.