Abstract:
Oxidative stress plays an important role in diabetes and other
oxygen-related diseases. Melatonin, a pineal hormone thought to be
a scavenger of oxygen radicals and a potentially advantageou s ther-
apeutic agent in diseases having oxidative stress, was administered
(10 mg / kg ip, in gum tragacanth to prolong its absorption, once
a day for 4 successive days) to normal and 30-day streptozotocin
induced diabetic Sprague-Dawley rats, after which markers of ox-
idative stress were assessed in the liver, kidney, intestine, and spleen.
Alanine and aspartate aminotransferase activities in serum, which
were increased after diabetes, were not increased further by melato-
nin administration, indicating that there was no melatonin-related
liver toxicity. Most melatonin-induced effects were seen in the liver,
and very few in extrahepatic tissues. In livers of diabetic rats, re-
duced concentration of nitrite and increased lipid peroxidation
were both restored to normal levels following treatment with mela-
tonin. Hepatic glutathione peroxidase activity was not changed
in diabetics, but was decreased after melatonin administration in
both normal and diabetic animals. Total glutathione concentra-
tions were signi® cantly decreased in livers of all diabetics and were
not normalized by melatonin treatment. Hepatic superoxide dis-
mutase activity was elevated following melatonin dosing in normal
rats, but dropped below normal levels in diabetic rats and was not
restored by melatonin treatment. Glutathione S -transferase activ-
ity was higher than normal in melatonin-dosed normal rat livers.
These results suggest that after 4 days of administration, melatonin
may enable various enzymes of the hepatic antioxidative defense
system to better detoxify harmful oxygen radicals without produc-
ing overt toxicity in a disease such as diabetes.
