December 2002
Volume 43, Issue 13
ARVO Annual Meeting Abstract  |   December 2002
Oxygen Damage To The Eye Lens
Author Affiliations & Notes
  • S Schaal
    Ophthalmology Rambam Medical Center Haifa Israel
  • A Dovrat
    B Rappaport Faculty of Medicine Technion Haifa Israel
  • I Beiran
    Ophthalmology Rambam Medical Center Haifa Israel
  • I Rubinstein
    B Rappaport Faculty of Medicine Technion Haifa Israel
  • B Miller
    Ophthalmology Rambam Medical Center Haifa Israel
  • Footnotes
    Commercial Relationships   S. Schaal, None; A. Dovrat, None; I. Beiran, None; I. Rubinstein, None; B. Miller, None.
Investigative Ophthalmology & Visual Science December 2002, Vol.43, 2368. doi:
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    • Get Citation

      S Schaal, A Dovrat, I Beiran, I Rubinstein, B Miller; Oxygen Damage To The Eye Lens . Invest. Ophthalmol. Vis. Sci. 2002;43(13):2368.

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

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Abstract: : Purpose: To investigate the damage caused by oxygen to the eye lens. Methods:170 bovine lenses were placed in specially designed culture containers and were divided into 5 groups. (1) Control group. (2) Group treated by a single exposure to hyperbaric oxygen: 100% oxygen in a pressure chamber at 2.5 absolute atmospheres (ATA). (3) Group treated daily by hyperbaric oxygen for 4 days. (4) Group treated daily for 4 days by normobaric oxygen:100% oxygen at 1 ATA. (5) Group treated daily for 4 days by hyperbaric air: 8.4% oxygen at 2.5 absolute atmospheres (ATA). Exposure time for all experimental groups was 120 minutes. Lens optical quality was assessed throughout the 7 days of the culture period and lens epithelial samples were taken each day for catalase activity analysis. Results:The lenses in the control group, the single hyperbaric oxygen exposure group and the hyperbaric air exposure group maintained their optical quality throughout the 7 days in culture. Repetitive exposures to both hyperbaric and normobaric oxygen caused optical damage to the lenses. Damage was more severe in the hyperbaric oxygen exposure group compared to the normobaric oxygen exposure group. The lenticular optical damage progressed from the lens periphery to its center. Lenticular catalase activity was affected by exposure to hyperbaric oxygen. Conclusion:Oxygen damage to bovine lenses was demonstrated in our model. According to our results it seems that oxygen-induced lenticular damage is a cumulative process depending on both length of exposure and on oxygen partial pressure. The enzyme catalase may play a role in hyperbaric oxygen-induced lenticular damage.

Keywords: 338 cataract • 399 enzymes/enzyme inhibitors • 504 oxidation/oxidative or free radical damage 

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