Biomedical Engineering Reference
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the liver at through out the 7 days. TBA was increased in the
brain, almost doubling by 7 days with increases seen in the liver
forupto5days.
These observations support a decrease in antioxidant activity in the
brain and liver following very high oral methanol dosing in rats. The
oxidative mechanism in the brain and liver appear to be different. In
the liver, peroxide is primarily removed by CAT, while GSH-Px is more
important in the brain (Skrzydlewska et al., 1998).
In another study, the effect of antioxidants (triolox derivative
U-83836E and N-acretylcystiene) were evaluated on lipid peroxidation
in erythrocytes of methanol-treated rats. Previous work has demon-
strated that methanol ingestion in rats increased lipid peroxidation of
erythrocytes. Intraperitoneal injects of these antioxidants (triolox deriv-
ative U-83836E and N-acretylcystiene) in rats receiving 3.0 gm/kg of
methanol orally, partially prevent lipid peroxidation in the erythrocytes.
These effects may be due to the effect of these added antioxidants on the
production of ROS (Dobrzyska et al., 1999).
In a short-term repeat study in rats, the effect of methanol on
antioxidant status and lipid peroxidation in the lymphoid organs
(lymph glands, spleen, thymus, and bone marrow) in male Wistar
rats (180-200 g/bw) was investigated following 2.37 g/kg bw (25%
LD 50 ) intraperitoneally for 1, 15, or 30 days. Repeated dose of 3.16
or 4.74 gm/kg bw intraperitoneally for 15 days or more resulted in
mortality. Lipid peroxidation was estimated by determining MDA and
was elevated at each time period (higher with increase time of treat-
ment) in the lymph nodes, spleen, thymus, and bone marrow.
All enzymatic (superoxide dismutase, CAT, and glutathione peroxi-
dase) and nonenzymatic antioxidant (reduced glutathione and vitamin
C) were significantly elevated following 1-day treatment in thymus,
spleen, lymph nodes, and bone marrow, but these indices were signifi-
cantly lower than the control on day 15 and lower still on day 30 also
indicate oxidative damage on the immune cells of the lymphoid organs.
When free radical increases as a result of methanol treatment, it appears
that endogenous antioxidant enzymes increase to remove the free
radicals and prevent oxidative damage. When the antioxidant defense
mechanism is overwhelmed by free radicals, an increase in lipid
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