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The retina is the only part of the central nervous system that is exposed to light radiation between 400 and 780 nm. Short wavelength light (SWL) ranging between 400 and 480 nm are absorbed maximally by chromophores located in mitochondria. An abundance of mitochondria are located in retinal ganglion cell (RGC) intraocular axons and photoreceptor inner segments and as a consequence SWL will impact these organelles. The purpose of this article is to summarise the experimental evidence for the possible negative effects of SWL on RGC mitochondria, in situ. The threat of damage to photoreceptor mitochondria may be less than to RGCs, since macular carotenoid, located chiefly in Henle's layer of the photoreceptor inner segment absorbs SWL. The article underlines the hypothesis that SWL contributes to RGC death when these neurones are not in an optimum homoeostatic state as is likely to occur in conditions such as glaucoma and possibly other types of pathologies and even old age. A case therefore exists for the idea that shielding RGCs to slow down visual loss in certain circumstances. This can theoretically be achieved with lenses that reduce transmission of SWL but specifically allow for maximal transmission of 479 nm11Although the peak wave length of melanopsin is around 479nm even filtering out SWL of up to 485nm will still allow for sufficient stimulation of melanopsin. light to stimulate melanopsin and maintain an optimum sleep/wake cycle.
•The healthy retina is unaffected by short wavelength light (400–480 nm).•Short wavelength light negatively affects mitochondrial functions in laboratory experiments.•Retinal ganglion cell intraocular axons are laden with mitochondria.•Short wavelength light likely to have a negative effect on ganglion cells when mitochondria already affected.•Shielding ganglion cell mitochondria from specific wavelengths of light might slow down visual loss as in glaucoma.