Pierrette Dayhaw-Barker
Journal: International journal of toxicology 2003;21(6):451-4
PMID: 12537641
Ocular morphology is specifically directed at facilitating the transmittance of visible light to the retina for the purposes of photoreceptor absorption and phototransduction, thereby initiating the process of vision. By absorbing excess radiation, melanin significantly enhances this process. It can also act as a photoprotector by quenching reactive oxygen species and other radicals produced as a result of the high oxygen dependency of the retina for its metabolism. However, melanin also binds numerous pharmaceuticals, a process that can result in ocular toxicity. Although our understanding of this binding remains somewhat limited, melanin chemistry, its distribution, and other factors influencing binding appear to play a significant role in predisposing ocular tissues, such as the choroid and retinal pigment epithelium, to toxicological insult. Many of the drugs that have been identified as causing these effects are known photosensitizers in which radiation plays a significant role in eliciting the pathologies. The phototoxic effects range from minor histological/chemical changes, which do not impact the quality of vision, to pigmentary retinopathies, which could potentially involve the loss of sight. Such effects, resulting from photosensitizer-drug binding to melanin, are to be separated from toxic effects, such as some ganglion cell abnormalities, that result from pharmaceuticals affecting ocular tissues directly.
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