Molecular mechanisms of light damage to the eye and its treatment

摘要

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 mechanism 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 10$+6$/ M$+$MIN@1$/ s$+$MIN@1$/; hydroxyl radical is scavenged at a rate of 10$+9$/ M$+$MIN@1$/ s$+$MIN@1$/ and superoxide is scavenged at a rate of 10$+3$/ M$+$MIN@1$/ s$+$MIN@1$/. In addition thiols block nitric oxide 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.!47