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EFFECT OF MELATONIN INJECTIONS ON THE GLUTATHIONE SYSTEM IN HEART TISSUE OF RATS UNDER EXPERIMENTAL DIABETES
I Yaremii1, O Kushnir1, Yu Vepriuk1
1Higher State Educational Establishment of Ukraine "Bukovinian State Medical University", Chernivtsi, Ukraine.
Georgian Medical News
|July 17, 2020
Summary
Melatonin treatment reduced blood glucose and stabilized antioxidant defense markers in the heart tissue of alloxan-induced diabetic rats. This study highlights melatonin
Area of Science:
- Biochemistry
- Endocrinology
- Pharmacology
Background:
- Alloxan-induced diabetes in rats leads to significant oxidative stress in heart tissue.
- Diabetic cardiomyopathy is characterized by altered glucose metabolism and antioxidant enzyme activity.
- Melatonin is a hormone with known antioxidant properties.
Purpose of the Study:
- To investigate the effect of melatonin on basal glucose levels and oxidative stress markers in the heart of diabetic rats.
- To assess the impact of melatonin on antioxidant defense systems, including glutathione and related enzymes.
Main Methods:
- Alloxan monohydrate was used to induce diabetes in rats.
- Experimental groups included control, diabetic, and diabetic rats treated with melatonin.
- Key biochemical parameters in heart tissue were measured: basal glucose, thiobarbituric acid reactive compounds (TBCRC), reduced glutathione (GSH), and activities of glutathione reductase (GR), glutathione peroxidase (GPx), and glucose-6-phosphate dehydrogenase (G-6-PhD).
Main Results:
- Diabetic rats exhibited significantly increased TBCRC levels and decreased GSH, GPx, G-6-PhD, and GR activity in heart tissue.
- Melatonin administration to diabetic rats resulted in a reduction in basal glucose levels.
- Melatonin treatment helped stabilize antioxidant defense indices, including TBCRC, GSH, GR, GPx, and G-6-PhD levels in the heart.
Conclusions:
- Melatonin demonstrates a protective effect against oxidative stress in the heart of diabetic rats.
- Melatonin may be a potential therapeutic agent for managing diabetic complications related to oxidative damage in cardiac tissue.

