Mitochondria and the regulation of free radical damage in the eye

Research output: Contribution to journalShort survey

4 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)145-148
Number of pages4
JournalJournal of Ocular Biology, Diseases, and Informatics
Volume2
Issue number3
DOIs
StatePublished - Sep 1 2009

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Free Radicals
Reactive Oxygen Species
Cell Survival
Mitochondria
Cistanche
Retinal Rod Photoreceptor Cells
Retinal Ganglion Cells
Mitochondrial Proteins
Oxidative Phosphorylation
Chinese Traditional Medicine
Mitochondrial Membranes
Neuroglia
Primates
Parkinson Disease
Retina
Protons
Membrane Proteins
Seizures
Cell Death
Neurons

All Science Journal Classification (ASJC) codes

  • Ophthalmology
  • Genetics

Cite this

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title = "Mitochondria and the regulation of free radical damage in the eye",
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.",
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Mitochondria and the regulation of free radical damage in the eye. / Barnstable, Colin.

In: Journal of Ocular Biology, Diseases, and Informatics, Vol. 2, No. 3, 01.09.2009, p. 145-148.

Research output: Contribution to journalShort survey

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