Protective effects of melatonin in experimental free radical-related ocular diseases.
Melatonin (N-acetyl-5-methoxytryptamine) is an indoleamine with a range of antioxidative properties. Melatonin is endogenously produced in the eye and in other organs. Current evidence suggests that melatonin may act as a protective agent in ocular conditions such as photo-keratitis, cataract, glaucoma, retinopathy of prematurity and ischemia/reperfusion injury. These diseases are sight-threatening and they currently remain, for the most part, untreatable. The pathogenesis of these conditions is not entirely clear but oxidative stress has been proposed as one of the causative factors. Elevated levels of various reactive oxygen and nitrogen species have been identified in diseased ocular structures. These reactants damage the structure and deplete the eye of natural defense systems, such as the antioxidant, reduced glutathione, and the antioxidant enzyme superoxide dismutase. Oxidative damage in the eye leads to apoptotic degeneration of retinal neurons and fluid accumulation. Retinal degeneration decreases visual sensitivity and even a small change in the fluid content of the cornea and crystalline lens is sufficient to disrupt ocular transparency. In the eye, melatonin is produced in the retina and in the ciliary body. Continuous regeneration of melatonin in the eye offers a frontier antioxidative defense for both the anterior and posterior eye. However, melatonin production is minimal in newborns and its production gradually wanes in aging individuals as indicated by the large drop in circulating blood concentrations of the indoleamine. These individuals are possibly at risk of contracting degenerative eye diseases that are free radical-based. Supplementation with melatonin, a potent antioxidant, in especially the aged population should be considered as a prophylaxis to preserve visual functions. It may benefit many individuals worldwide, especially in countries where access to medical facilities is limited.
Siu
Andrew W
AW
Department of Cellular and Structural Biology, University of Texas Health Science Center, San Antonio, TX, USA. sosiua@polyu.edu.hk
Maldonado
Maria
M
Sanchez-Hidalgo
Marina
M
Tan
Dun-Xian
DX
Reiter
Russel J
RJ
D000975:Antioxidants / Q000502:physiology*; D002386:Cataract / Q000503:physiopathology; D005128:Eye Diseases / Q000503:physiopathology*; D005901:Glaucoma / Q000503:physiopathology; D006801:Humans; D007634:Keratitis / Q000503:physiopathology; D008550:Melatonin / Q000502:physiology*; D009799:Ocular Physiological Phenomena; D015427:Reperfusion Injury / Q000503:physiopathology; D012164:Retinal Diseases / Q000503:physiopathology
D000975:Antioxidants; D008550:Melatonin