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Abstract
Numerous short-lived and highly reactive oxygen species (ROS) such as superoxide (O2(.-)),
hydroxyl radical, and hydrogen peroxide are continuously generated in vivo. Depending
upon concentration, location, and intracellular conditions, ROS can cause toxicity
or act as signaling molecules. The cellular levels of ROS are controlled by antioxidant
enzymes and small-molecule antioxidants. As major antioxidant enzymes, superoxide
dismutases (SODs), including copper-zinc superoxide dismutase (Cu/ZnSOD), manganese
superoxide dismutase, and extracellular superoxide dismutase, play a crucial role
in scavenging O2(.-). This review focuses on the regulation of the sod genes coding
for these enzymes, with an emphasis on the human genes. Current knowledge about sod
structure and regulation is summarized and depicted as diagrams. Studies to date on
genes coding for Cu/ZnSOD (sod1) are mostly focused on alterations in the coding region
and their associations with amyotrophic lateral sclerosis. Evaluation of nucleotide
sequences reveals that regulatory elements of the sod2 gene reside in both the noncoding
and the coding region. Changes associated with sod2 lead to alterations in expression
levels as well as protein function. We also discuss the structural basis for the changes
in SOD expression associated with pathological conditions and where more work is needed
to establish the relationship between SODs and diseases.