Protective Effects of
Melatonin on Myocardial Ischemia-Reperfusion Induced Infarct
Size and Oxidative Changes
E. SAHNA1, H. PARLAKPINAR2,
Y. TURKOZ3, A. ACET2
1Department of Pharmacology, Faculty of Medicine,
Firat University, Elazig, Turkey, 2Department of
Pharmacology, and 3Department of Biochemistry,
Faculty of Medicine, Inonu University, Malatya, Turkey
Received July 8, 2004
Accepted November 23, 2004
On-line available January 10, 2005
Summary
Free radicals, calcium overloading and loss of membrane
phospholipids play an important role in the development of
ischemia/reperfusion (I/R) injury. Melatonin is a well-known
antioxidant and free radical scavenger. Melatonin may also
reduce the intracellular calcium overloading and inhibit lipid
peroxidation. This study was designed to investigate the effects
of melatonin on the I/R-induced cardiac infarct size in an in
vivo rat model. We also investigated glutathione (GSH) levels,
an antioxidant the levels of which are influenced by oxidative
stress, and malondialdehyde (MDA) levels, which is an index of
lipid peroxidation. To produce cardiac damage, the left main
coronary artery was occluded for 30 min, followed by 120 min
reperfusion, in anesthetized rats. Melatonin (10 mg/kg) or
vehicle was given 10 min before ischemia via the jugular vein.
Infarct size, expressed as the percentage of the risk zone, was
found significantly greater in I/R group than in the
melatonin-treated I/R group. MDA levels were significantly
higher, but GSH levels were lower in the I/R group than in the
control group. Melatonin significantly reduced the MDA values
and increased the GSH levels. These results suggest that
oxidative stress contributes to myocardial I/R injury and
melatonin administration exerts a mitigating effect on infarct
size. Furthermore, the results indicated that melatonin improves
the antioxidant capacity of the heart and attenuates the degree
of lipid peroxidation after I/R.
Key words
Melatonin • Reperfusion injury • Heart • Infarct size •
Glutathione • Malondialdehyde
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