Oxidation of potassium channels by ROS: a general mechanism of aging and neurodegeneration?
A wealth of evidence underscores the tight link between oxidative stress, neurodegeneration and aging. When the level of excess reactive oxygen species (ROS) increases in the cell, a phenomenon characteristic of aging, DNA is damaged, proteins are oxidized, lipids are degraded and more ROS are produced, all culminating in significant cell injury. Recently we showed that in the nematode, Caenorhabditis elegans, oxidation of K(+) channels by ROS is a major mechanism underlying the loss of neuronal function. The C. elegans results support an argument that K(+) channels controlling neuronal excitability and survival might provide a common, functionally important substrate for ROS in aging mammals. Here we discuss the implications that oxidation of K(+) channels by ROS might have for the mammalian brain during normal aging, as well as in neurodegenerative diseases such as Alzheimer's and Parkinson's. We argue that oxidation of K(+) channels by ROS is a common theme in the aging brain and suggest directions for future experimentation.
Department of Physiology and Biophysics, University of Medicine and Dentistry of New Jersey, Robert Wood Johnson Medical School, 683 Hoes Lane, Piscataway, NJ 08854, USA. sestife@umdnj.edu
Federico
F
Sesti
Shuang
S
Liu
Shi-Qing
SQ
Cai
D000375:Aging; D000818:Animals; D006801:Humans; D009410:Nerve Degeneration / Q000378:metabolism*; D010084:Oxidation-Reduction; D015221:Potassium Channels / Q000378:metabolism*; D017382:Reactive Oxygen Species / Q000378:metabolism*
D015221:Potassium Channels; D017382:Reactive Oxygen Species