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Mitochondria and the regulation of free radical damage in the eye.
J Ocul Biol Dis Infor. 2009 Sep; 2(3):145-148.JO

Abstract

Neuronal cell death can be determined by the overall level of reactive oxygen species (ROS) resulting from the combination of extrinsic sources and intrinsic production as a byproduct of oxidative phosphorylation. Key controllers of the intrinsic production of ROS are the mitochondrial uncoupling proteins (UCPs). By allowing a controlled leak of protons across the inner mitochondrial membrane activation of these proteins can decrease ROS and promote cell survival. In both primate models of Parkinson's disease and mouse models of seizures, increased activity of UCP2 significantly increased neuronal cells survival. In the retina UCP2 is expressed in many neurons and glial cells, but was not detected in rod photoreceptors. Retinal ganglion cell survival following excitotoxic damage was much greater in animals overexpressing UCP2. Traditional Chinese medicines, such as an extract of Cistanche tubulosa, may provide benefit by altering mitochondrial metabolism.

Authors+Show Affiliations

Department of Neural and Behavioral Sciences, Penn State University College of Medicine, Hershey, PA 17033 USA.

Pub Type(s)

Journal Article

Language

eng

PubMed ID

20046847

Citation

Barnstable, Colin J.. "Mitochondria and the Regulation of Free Radical Damage in the Eye." Journal of Ocular Biology, Diseases, and Informatics, vol. 2, no. 3, 2009, pp. 145-148.
Barnstable CJ. Mitochondria and the regulation of free radical damage in the eye. J Ocul Biol Dis Infor. 2009;2(3):145-148.
Barnstable, C. J. (2009). Mitochondria and the regulation of free radical damage in the eye. Journal of Ocular Biology, Diseases, and Informatics, 2(3), 145-148.
Barnstable CJ. Mitochondria and the Regulation of Free Radical Damage in the Eye. J Ocul Biol Dis Infor. 2009;2(3):145-148. PubMed PMID: 20046847.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Mitochondria and the regulation of free radical damage in the eye. A1 - Barnstable,Colin J, Y1 - 2009/09/18/ PY - 2009/07/23/received PY - 2009/09/03/accepted PY - 2010/1/5/entrez PY - 2010/1/5/pubmed PY - 2010/1/5/medline SP - 145 EP - 148 JF - Journal of ocular biology, diseases, and informatics JO - J Ocul Biol Dis Infor VL - 2 IS - 3 N2 - Neuronal cell death can be determined by the overall level of reactive oxygen species (ROS) resulting from the combination of extrinsic sources and intrinsic production as a byproduct of oxidative phosphorylation. Key controllers of the intrinsic production of ROS are the mitochondrial uncoupling proteins (UCPs). By allowing a controlled leak of protons across the inner mitochondrial membrane activation of these proteins can decrease ROS and promote cell survival. In both primate models of Parkinson's disease and mouse models of seizures, increased activity of UCP2 significantly increased neuronal cells survival. In the retina UCP2 is expressed in many neurons and glial cells, but was not detected in rod photoreceptors. Retinal ganglion cell survival following excitotoxic damage was much greater in animals overexpressing UCP2. Traditional Chinese medicines, such as an extract of Cistanche tubulosa, may provide benefit by altering mitochondrial metabolism. SN - 1936-8437 UR - https://www.unboundmedicine.com/medline/citation/20046847/Mitochondria_and_the_regulation_of_free_radical_damage_in_the_eye_ L2 - https://dx.doi.org/10.1007/s12177-009-9036-4 DB - PRIME DP - Unbound Medicine ER -
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