November 2013
Volume 54, Issue 12
Research Highlight  |   November 2013
Reversing the Age-Dependent Decline in Lens Transport: A New Strategy to Prevent Age Related Nuclear Cataract?
Investigative Ophthalmology & Visual Science November 2013, Vol.54, 7188. doi:
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      Paul Donaldson; Reversing the Age-Dependent Decline in Lens Transport: A New Strategy to Prevent Age Related Nuclear Cataract?. Invest. Ophthalmol. Vis. Sci. 2013;54(12):7188.

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      © ARVO (1962-2015); The Authors (2016-present)

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It is now well accepted that the dense central opacity typically observed in age-related nuclear cataract is caused by oxidative damage to crystallin proteins, which in turn causes them to aggregate and scatter light as it passes through the lens nucleus. These findings have led to the hypothesis that oxidizing agents are the causal factors in the initiation of age-related nuclear cataract. 1 However, oxidative damage—at least in young lenses—is prevented by a number of powerful scavenger systems and chaperone molecules. 2 Furthermore, molecular O2 is consumed by mitochondria and other systems, keeping its concentration near zero in the central fiber cells of normal lenses. 3 These systems would need to be first compromised in the lens nucleus of older lenses in order to produce the extensive oxidative damage seen in age-related cataract. This leads to the question of whether oxidative damage is causal or consequential to some other changes that lead to a loss of homeostasis in central fiber cells. Evidence for the latter has been produced in a paper published by Gao and colleagues. 4 In this article, they show that with advancing age there is a downregulation of gap junction coupling, a depolarization of the intracellular voltage, and increases in the intracellular concentrations of both sodium and calcium that reduce the transmembrane driving force for the uptake of key nutrients and antioxidants by sodium-dependent membrane transporters. 4 Thus with advancing age, the underlying physiology of the lens—and therefore its ability to maintain an environment that protects nuclear proteins against oxidative stress—deteriorates, resulting in increased oxidative damage, crystallin aggregation, and ultimately increased light scattering. These findings suggest that enhancing the physiology of the aging lens and its ability to deliver and effectively utilize antioxidant supplements will be a key strategy for the development of novel therapies to reduce the incidence of age-related nuclear cataract. 
Truscott RJ. Human cataract: the mechanisms responsible; light and butterfly eyes. Int J Biochem Cell Biol . 2003; 35: 1500–1504. [CrossRef] [PubMed]
Bron AJ Vrensen GF Koretz J Maraini G Harding JJ. The ageing lens. Ophthalmologica . 2000; 214: 86–104. [CrossRef] [PubMed]
McNulty R Wang H Mathias RT Ortwerth BJ Truscott RJ Bassnett S. Regulation of tissue oxygen levels in the mammalian lens. J Physiol . 2004; 559 (pt 3): 883–898. [CrossRef] [PubMed]
Gao J Wang H Sun X The effects of age on lens transport. Invest Ophthalmol Vis Sci . 2013; 54: 7174–7187. [CrossRef] [PubMed]

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