<title>Molecular mechanisms of light damage to the eye and its treatment</title>

Abstract

The eye is continually subjected to ambient radiation. The benign function of this light is to direct vision and circadian rhythm. However, under intense light from artificial sources such as lasers and operating room microscopes the natural protection of eye against light damage may be undermined. The damage can be a result of a photochemical, thermal or mechanical injury which can all disrupt ocular tissues . The mechani sm for the above damage involves the production free radical and reactive oxygen intermediates either as a primary effect of the absorbance of the light or as a secondary effect due to an inflammatory response to heat or mechanical injury. This can induce a cytokine cascade as well as induce the increased production of nitric oxide.Glutathione mimics can block light induced free radical and oxygen radical intermediates in the eye. For instance, singlet oxygen is scavenged at a rate of 106 M1 s1 hydroxyl radical is scavenged at a rate of l0 W1 S-and superoxide is scavenged at a rate of 10 M1 s 1 In addition thiols block nitric oxide (NO) and other intermediates involved in an inflammatory response. Glutathione mimics which have offered in vivo protection against light damage to the lens and retina, have the potential to protect against laser-induced damage to the human eye.

Light-induced Damage in the Retina: Differential Effects of Dimethylthiourea on Photoreceptor Survival, Apoptosis and DNA Oxidation

“…In this paper we explore possible interrelationships between DNA oxidation, apoptosis and net loss of photoreceptors, by taking advantage of the ability of the antioxidant DMTU to protect albino rats against light-induced photoreceptor death (4). Because DMTU is a thiol it may have properties similar to glutathione that efficiently quenches hydroxyl radical (25). Under a regimen of light exposure leading to similar degrees of cell death in dark-and dim lightreared rats, we have noted a marked difference in the kinetics of DNA fragmentation between the two rearing conditions.…”

“…Although apoptosis and necrosis may simply coexist as unrelated components of retinal light damage, it is tempting to speculate that the two phenomena are biologically coupled. Another explanation for our findings may relate to the relative ability of DMTU to quench reactive oxygen species or reactive nitrogen species (25). It is entirely possible that one form of oxidant is produced in higher concentration in the dim-light-or dark-reared rats and that DMTU, while effective, is less able to completely block different oxidative processes in the different types of rats.…”

“…The synthetic antioxidant DMTU provides a powerful experimental tool for examining the relative importance of various cellular phenomena in this process because, in our albino rat model system, it prevents photoreceptor cell loss after light exposures that would otherwise destroy the cells (4). Thus, oxidative events that are linked to retinal light damage could be expected to be affected by the administration of DMTU, or other antioxidants (25). to the experimental animal.…”