April 2011
Volume 52, Issue 14
ARVO Annual Meeting Abstract  |   April 2011
Arsenic And Cataract
Author Affiliations & Notes
  • Norman J. Kleiman
    Environmental Health Sciences, Columbia University, New York, New York
  • Kara G. Fields
    Environmental Health Sciences, Columbia University, New York, New York
  • Adrienne M. Quinn
    Environmental Health Sciences, Columbia University, New York, New York
  • Vesna Slavkovich
    Environmental Health Sciences, Columbia University, New York, New York
  • Joseph Graziano
    Environmental Health Sciences, Columbia University, New York, New York
  • Footnotes
    Commercial Relationships  Norman J. Kleiman, None; Kara G. Fields, None; Adrienne M. Quinn, None; Vesna Slavkovich, None; Joseph Graziano, None
  • Footnotes
    Support  NIEHS Grant P30ES009089 (NJK), Fight for Sight Summer Student Fellowship (KGF)
Investigative Ophthalmology & Visual Science April 2011, Vol.52, 796. doi:
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      Norman J. Kleiman, Kara G. Fields, Adrienne M. Quinn, Vesna Slavkovich, Joseph Graziano; Arsenic And Cataract. Invest. Ophthalmol. Vis. Sci. 2011;52(14):796.

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

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Purpose: : Exposure to elevated concentrations of arsenic in drinking water is a major human health problem in much of the world. Arsenic poisoning of groundwater in Bangladesh affects the health of tens of millions of individuals and may be the largest mass poisoning in history. Oxidative stress mechanisms and/or reactive oxygen species are implicated in arsenic carcinogenicity and genotoxicity. Oxidative stress is also believed to be an initiating or early event in cataractogenesis. We hypothesize that elevated exposure to arsenic may be a contributing factor in lens opacification. A pilot study was initiated to determine if elevated arsenic could be detected in eye tissue of mice chronically exposed to sodium arsenate or sodium arsenite in their drinking water.

Methods: : Ocular concentrations of elemental arsenic were determined by ICP/Mass Spectroscopy and compared to liver, heart, lung, kidney, brain, skin and hair samples from C57BL6 mice given either 10 or 50 ppm Na arsenite or Na arsenate in their drinking water for up to 4 months. At various time points after exposure, animals were sacrificed, selected organs and tissues removed and completely digested for elemental arsenic determinations. Organs and tissues from control mice, unexposed to arsenic, were similarly examined.

Results: : A dose and time dependent increase in arsenic could be detected in eyes of mice given arsenic in their drinking water. The majority of ocular arsenic is found in lens as compared to other eye tissues. Lens levels of arsenic are roughly half that found in kidney and significantly higher than that in many other tissues and organs. For example, As concentrations after 4 months chronic exposure to 50 ppm Na arsenite are: Hair: 38.3 ug/g, Kidney: 4.6 ug/g, Eye: 2.7 ug/g, Skin: 0.5 ug/g, Lung: 0.48 ug/g, Liver: 0.435 ug/g, Heart: 0.23 ug/g and brain: 0.139 ug/g. Na arsenite appears more effectively concentrated in eye and other tissues than Na arsenate.

Conclusions: : The relatively high concentrations of arsenic detected in lens after chronic exposure to arsenite or arsenate in drinking water supports the hypothesis that human exposure to elevated levels of As in drinking water could induce oxidative stress in the lens and be a contributing factor in lens opacification.

Keywords: oxidation/oxidative or free radical damage 

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