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Role of free Radicals

Cataracts

Cataracts are one of the major causes of blindness worldwide. The disease affects up to 50% of the population over 75 years of age in the USA, with a greater incidence in developing nations. The lens has substantial supplies of antioxidant reserves, antioxidant enzymes and secondary defenses, to prevent cataract formation. Exposure to environmental stress, such as UV light, smoking and oxygen results in the production of radical species, which damage lens proteins. Superoxide and hydroxyl radicals cause damage to cell membrane lipids and proteins, which deposit on the surface of the lens causing opacities. Decreased levels of ascorbate and -carotene, and increased incidence of cataract formation, have been reported in smokers. This increased exposure to oxidative stress and decreased antioxidant protection is thought to contribute to the increased incidence of the disease. Many epidemiological studies have examined the association between cataract formation and nutrition. High nutritional intake of vitamin E, C and -carotene, associated with a decreased risk of cataract formation. Ascorbate levels in the lens are significantly higher than plasma levels and vitamin C is reportedly the most effective grade at reducing cataract incidence. One study described a 70 % lower incidence of cataract formation in individuals supplemented with vitamin C compared to those without vitamin C-supplementation.

References

  1. Thiagarajan G. Chandani S. Sundari CS. Rao SH. Kulkarni AV. Balasubramanian D. Antioxidant properties of green and black tea, and their potential ability to retard the progression of eye lens cataract. Experimental Eye Research. 73(3):393-401, 2001

  2. Cameron MD. Poyer JF. Aust SD. Identification of free radicals produced during phacoemulsification. Journal of Cataract & Refractive Surgery. 27(3):463-70, 2001

  3. Kumagai Y. Wakayama T. Lib S. Shinohara A. Iwamatsu A. Sun G. Shimojo N. Zeta-crystallin catalyzes the reductive activation of 2,4,6-trinitrotoluene to generate reactive oxygen species: a proposed mechanism for the induction of cataracts.FEBS Letters. 478(3):295-8, 2000

  4. Gracy RW. Talent JM. Kong Y. Conrad CC. Reactive oxygen species: the unavoidable environmental insult?.Mutation Research. 428(1-2):17-22, 1999

  5. Linetsky M. James HL. Ortwerth BJ. Spontaneous generation of superoxide anion by human lens proteins and by calf lens proteins ascorbylated in vitro. Experimental Eye Research. 69(2):239-48, 1999

  6. Zhao W. Devamanoharan PS. Varma SD. Fructose induced deactivation of glucose-6-phosphate dehydrogenase activity and its prevention by pyruvate: implications in cataract prevention. Free Radical Research. 29(4):315-20, 1998

  7. Diplock AT. Charleux JL. Crozier-Willi G. Kok FJ. Rice-Evans C. Roberfroid M. Stahl W. Vina-Ribes J. Functional food science and defence against reactive oxidative species. British Journal of Nutrition. 80 Suppl 1:S77-112, 1998

  8. Spector A. Ma W. Wang RR. Kleiman NJ. Microperoxidases catalytically degrade reactive oxygen species and may be anti-cataract agents. Experimental Eye Research. 65(4):457-70, 1997

  9. Bhuyan DK. Huang X. Kuriakose G. Garner WH. Bhuyan KC. Menadione-induced oxidative stress accelerates onset of Emory mouse cataract in vivo. Current Eye Research. 16(6):519-26, 1997

  10. Bhuyan DK. Master RW. Bhuyan KC. Crosslinking of aminophospholipids in cellular membranes of lens by oxidative stress in vitro. Biochimica et Biophysica Acta. 1285(1):21-8, 1996

  11. Guglielmotti A. Capezzone De Joannon A. Cazzolla N. Marchetti M. Soldo L. Cavallo G. Pinza M. Radical scavenger activity of bendazac, an anticataract non-steroidal anti-inflammatory agent.Pharmacological Research. 32(6):369-73, 1995

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