PT - JOURNAL ARTICLE AU - Neelam, Kumari AU - Goenadi, Catherina J AU - Lun, Katherine AU - Yip, Chee Chew AU - Au Eong, Kah-Guan TI - Putative protective role of lutein and zeaxanthin in diabetic retinopathy AID - 10.1136/bjophthalmol-2016-309814 DP - 2017 May 01 TA - British Journal of Ophthalmology PG - 551--558 VI - 101 IP - 5 4099 - http://bjo.bmj.com/content/101/5/551.short 4100 - http://bjo.bmj.com/content/101/5/551.full SO - Br J Ophthalmol2017 May 01; 101 AB - Diabetic retinopathy (DR) is one of the most important microvascular complications of diabetes and remains the leading cause of blindness in the working-age individuals. The exact aetiopathogenesis of DR remains elusive despite major advances in basic science and clinical research. Oxidative damage as one of the underlying causes for DR is increasingly being recognised. In humans, three hydroxycarotenoids, lutein (L), zeaxanthin (Z) and meso-zeaxanthin (MZ), accumulate at the central retina (to the exclusion of all other dietary carotenoids), where they are collectively known as macular pigment. These hydroxycarotenoids by nature of their biochemical structure and function help neutralise reactive oxygen species, and thereby, prevent oxidative damage to the retina (biological antioxidants). Apart from their key antioxidant function, evidence is emerging that these carotenoids may also exhibit neuroprotective and anti-inflammatory function in the retina. Since the preliminary identification of hydroxycarotenoid in the human macula by Wald in the 1940s, there has been astounding progress in our knowledge of the role of these carotenoids in promoting ocular health. While the Age-Related Eye Disease Study 2 has established a clinical benefit for L and Z supplements in patients with age-related macular degeneration, the role of these carotenoids in other retinal diseases potentially linked to oxidative damage remains unclear. In this article, we comprehensively review the literature germane to the putative protective role of two hydroxycarotenoids, L and Z, in the pathogenesis of DR.