Wmu. Daniels et al., MELATONIN COUNTERACTS LIPID-PEROXIDATION INDUCED BY CARBON-TETRACHLORIDE BUT DOES NOT RESTORE GLUCOSE-6 PHOSPHATASE-ACTIVITY, Journal of pineal research, 19(1), 1995, pp. 1-6
Carbon tetrachloride (CCl4) exerts its toxic effects by the generation
of free radicals. In this study we investigated whether melatonin, a
potent free radical scavenger, could prevent the deleterious effects o
f CCl4. Liver homogenates and liver microsomes were incubated with CCl
4 in the presence of melatonin and lipid peroxidation and glucose-6 ph
osphatase (G6Pase) activity were determined. All doses of CCl4 (1, 0.5
, 0.1 mM) produced significantly high levels of lipid peroxidation, as
reflected by increased levels of malonaldehyde and 4-hydroxyalkenals,
in both liver homogenates and liver microsomes. These doses of CCl4 c
oncommitantly reduced the activity of microsomal G6Pase. Go-incubation
with melatonin dose-dependently (2, 1, 0.5 mM) inhibited the producti
on of lipid peroxidation, but it was unable to restore the activity of
G6Pase. In in vivo studies, rats were also treated with melatonin (10
mg/kg, i.p.), given 30 min before and 60 min after the administration
of CCl4 (5 ml/kg, i.p.). Significantly elevated levels of lipid perox
idation were measured in the liver and kidney. Melatonin prevented the
CCl4-induced lipid peroxidation in the kidney, bur not in the liver.
These data suggest that melatonin may provide protection against some
of the damaging effects of CCl4, possibly due to its ability to scaven
ge toxic free radicals.