The enzyme
super oxide dismutase catalyzes the dismutation of superoxide into oxygen and
hydrogen peroxide (chaki et al, 2006). As such, it is an important antioxidant
defense in nearly al cells exposed to oxygen. In humans, three forms of
superoxide dismutase are present. SOD I is located in the cytoplasm, SOD 2 in
the mitochondria and SOD 3 is extra cellular (chaki et al, 2006). The first
is a dimer (consists of two units), while the others are tetramers (four
subunits). SOD 1 and SOD 3 contain copper and zinc, while SOD 2 has manganese
in its reactive center. The genes are located on chromosomes 21, 6 and 4
respectively (Cao et al, 2008).
BIOCHEMISTRY
OF SUPER OXIDE DISMUTASE (SOD)
Simply
stated, SOD out competes damaging reactions of superoxide thus protecting the
cell from superoxide toxicity (Cao et al, 2008).In biological systems, its main
reactions are with itself (dismutation) or with another biological radical such
as nitric oxide (NO). Superoxide
is one of the main reactive oxygen species in the cell and as such, SOD serves
a key antioxidant role (chaki et al, 2006). The
physiological importance of SOD is illustrated by the severe pathologies
evident in mice genetically engineered to lack these enzymes. Mice lacking SOD
2 dies several days after birth amidst massive oxidative stress (Cao et al,
2008).Mice lacking SOD 1 develop a wide range of pathologies, including
hepatocellular carcinoma (an acceleration of age – related muscle mass loss),
an earlier incidence of cataracts and a reduced life span (Chaki et al, 2006). Mice
lacking SOD 3 do not show any obvious defects and exhibits a normal lifespan,
though they are move sensitive to hyperoxic injury (Chaki et al, 2006).
ROLE OF
SUPER OXIDE DISMUTASE (SOD) IN DISEASE
Mutations
in the SOD enzyme (SOD 1) can cause familial amyotrophic lateral sclerosis
(ALS) a form of motor neuron disease (Cao et al, 2008). SOD has
proved to be highly effective in treatment of colonic inflammation in
experimental colitis. Treatment with SOD decreases reactive oxygen species
generation and oxidative stress