Biomedical Engineering Reference
In-Depth Information
oral methanol dosing (6mg/kg bw) in rats has also been reported
(Skrzydlewska et al., 1998).
The effect of methanol on antioxidant status and lipid peroxidation in
the lymphoid organs (lymph glands, spleen, thymus, and bone marrow)
was investigated following a dose of 2.37 gmethanol/kg bw intra-
peritoneally (i.p.) for 1, 15, or 30 days. Lipid peroxidation was elevated
at each time period (higher with increase time of treatment). All
enzymatic and nonenzymatic antioxidant indices were significantly
elevated following 1-day treatment, but these indices were significantly
lower than the control on day 15 and lower still on day 30 indicating
oxidative damage to the thymus, spleen, lymph nodes, and bone marrow
(Parthasarathy et al., 2006).
Intraperitoneal injects of antioxidants (triolox derivative U-83836E
and N-acretylcystiene) in rats receiving 3.0 g/kg of methanol orally,
partially prevent lipid peroxidation in the erythrocytes demonstrating
the protective role of the added antioxidant on oxidative damage caused
by methanol (Dobrzynska et al., 1999).
In another study, an increase in the formation of free radicals in
Sprague Dawley rats was detected by electron spin resonance spectros-
copy following a single dose of methanol (i.p. 4.5 g/kg or gavage
7 g/kg). The same free radical adduct was detected in the bile and
urine 2 hours after dosing (Kadiiska and Mason, 2000).
In still another study, hydroxymethyl radicals were detected in rat
liver microsomes and nuclei of NADPH-dependent process following
treatment with methanol. The results suggest that both rat liver nuclei
and microsomes are able to generate free radicals during NADPH-
mediated methanol metabolism (Castro et al., 2002).
A study of mice, rabbits, and primates given a single or 15 daily doses
of 2.0 g of methanol i.p., (high enough to cause lipid peroxidation in
rats) was conducted to assess tissue oxidative DNA damage only.
Oxidative DNA damage is most commonly indicated by an increase
in 8-oxo-7, 8-dihydro-2
0
-deoxyguanosine (8-oxodG). 8-oxodG is muta-
genic and a potential cause of cancer. No increase in DNA damage (8-
oxodG) was noted in the spleen, liver, lung, bone marrow, or kidney in
mice, rabbits, or primates given a single dose of 2.0 g of methanol i.p.
However, an increase in hydroxynonenal-histidine (HNE-His) protein
