Role of exogenous melatonin on adriamycin-induced changes in the rat heart.
ABSTRACT The protective effect of melatonin on adriamycin (ADM)-induced cardiotoxicity was investigated in the rat heart. Melatonin is a pineal hormone with free radical scavenging activity on oxidants; therefore it may decrease the ADM-induced oxidative stress and cardiotoxicity so that therapeutic efficacy might be enhanced.
Wistar rats in 4 groups were treated with saline (control), melatonin (MEL), adriamycin (ADM) and melatonin plus adriamycin (MEL+ADM).
Adriamycin given at a single dose of 15 mg/kg significantly increased lipid peroxidation products as measured by thiobarbituric acid reactive substances (TBARS). Melatonin (5 mg/kg bw) given 2 days before and 7 days after ADM treatment reduced TBARS level. Adriamycin significantly reduced superoxide dismutase activity which was elevated by melatonin treatment. Additionally, ADM significantly increased catalase enzyme activity while melatonin normalized the ADM induced alteration in activity of catalase.
The combined use of ADM and melatonin reduces the threat of cardiomyopathy. Melatonin seems to hold promise as a therapeutic treatment and can be recommended as an adjunct in antitumor therapy as a safe and effective protection against acute ADM-induced cardiotoxicity.
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ABSTRACT: The review analyzed morphology, molecular and functional aspects of pineal gland aging and methods of it correction. The pineal gland is central organ, which regulates activity of neuroimmunoendocrine, antioxidant and other organisms systems. Functional activity of pineal gland is discreased at aging, which is the reason of melatonin level changing. The molecular and morphology research demonstrated, that pineal gland hadn't strongly pronounced atrophy at aging. Long-term experience showed, that peptides extract of pineal gland epithalamin and synthetic tetrapeptide on it base epithalon restored melatonin secretion in pineal gland and had strong regulatory activity at neuroimmunoendocrine and antioxidant organism systems.Fiziologiia cheloveka 01/2012; 38(1):119-27. DOI:10.1134/S0362119712010112