Oxidative stress, lens gap junctions, and cataracts
The eye lens is constantly subjected to oxidative stress from radiation and other sources. The lens has several mechanisms to protect its components from oxidative stress and to maintain its redox state, including enzymatic pathways and high concentrations of ascorbate and reduced glutathione. With...
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| Published in | Antioxidants & redox signaling Vol. 11; no. 2; p. 339 |
|---|---|
| Main Authors | , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.02.2009
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| Subjects | |
| Online Access | Get more information |
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| Abstract | The eye lens is constantly subjected to oxidative stress from radiation and other sources. The lens has several mechanisms to protect its components from oxidative stress and to maintain its redox state, including enzymatic pathways and high concentrations of ascorbate and reduced glutathione. With aging, accumulation of oxidized lens components and decreased efficiency of repair mechanisms can contribute to the development of lens opacities or cataracts. Maintenance of transparency and homeostasis of the avascular lens depend on an extensive network of gap junctions. Communication through gap junction channels allows intercellular passage of molecules (up to 1 kDa) including antioxidants. Lens gap junctions and their constituent proteins, connexins (Cx43, Cx46, and Cx50), are also subject to the effects of oxidative stress. These observations suggest that oxidative stress-induced damage to connexins (and consequent altered intercellular communication) may contribute to cataract formation. |
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| AbstractList | The eye lens is constantly subjected to oxidative stress from radiation and other sources. The lens has several mechanisms to protect its components from oxidative stress and to maintain its redox state, including enzymatic pathways and high concentrations of ascorbate and reduced glutathione. With aging, accumulation of oxidized lens components and decreased efficiency of repair mechanisms can contribute to the development of lens opacities or cataracts. Maintenance of transparency and homeostasis of the avascular lens depend on an extensive network of gap junctions. Communication through gap junction channels allows intercellular passage of molecules (up to 1 kDa) including antioxidants. Lens gap junctions and their constituent proteins, connexins (Cx43, Cx46, and Cx50), are also subject to the effects of oxidative stress. These observations suggest that oxidative stress-induced damage to connexins (and consequent altered intercellular communication) may contribute to cataract formation. |
| Author | Berthoud, Viviana M Beyer, Eric C |
| Author_xml | – sequence: 1 givenname: Viviana M surname: Berthoud fullname: Berthoud, Viviana M email: vberthou@peds.bsd.uchicago.edu organization: Department of Pediatrics, University of Chicago, Chicago, Illinois 60637, USA. vberthou@peds.bsd.uchicago.edu – sequence: 2 givenname: Eric C surname: Beyer fullname: Beyer, Eric C |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/18831679$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Cataract - metabolism Cataract - pathology Gap Junctions - metabolism Gap Junctions - physiology Humans Lens, Crystalline - metabolism Lens, Crystalline - pathology Models, Biological Oxidative Stress - physiology |
| Title | Oxidative stress, lens gap junctions, and cataracts |
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