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Acta Physiologica 2011; Volume 203, Supplement 686
Joint Congress of FEPS and Turkish Society of Physiological Sciences
9/3/2011-9/7/2011
Istanbul, Turkey
PROTECTIVE EFFECTS OF MELATONIN ON HEART TISSUE IN PINEALECTOMIZED RATS
Abstract number: PC272
Polat1 Alaadin, Parlakpinar2 Hakan, Tasdemir2 Seda, Acet2 Ahmet
1Innniversitesi Tp Fakltesi Fizyoloji Anabilim Dal
2Innniversitesi Tp Fakltesi Farmakoloji Anabilim Dal
Objective:
In the free radical theory of aging, it is suggested that accumulated free radical damage may be responsible for the degenerative process during aging. It is known that there is a reduction in serum melatonin concentration during aging. This situation may cause damage in the heart tissue, which is one of the more perfusing organs. The aim of the current study was to expose rats to an aging process via surgical pinealectomy (Px). For this, the effects of lack of chronic physiological melatonin on heart tissue were observed in the current study.
Methods:
The animals were divided into three groups. Group I and group II were designated as sham and Px rats. They were housed for 5 months before the beginning of treatment. Rats in group III were (denoted as) Px and melatonin was injected with 4 mg/kg/day (i.p.) for 28 days. Changes in oxidant substances were evaluated, especially those in lipid peroxidation, nitric oxide (NO), reduced glutathione (GSH) content and SOD activity levels during this period so that the antioxidant effects of long-term exogenous melatonin could be investigated.
Results:
In Px group, MDA and NO levels were found as elevated when compared with the sham group. The Px group exhibited reduced SOD activity and GSH content. All of these harmful changes were restored by melatonin supplementation.
Conclusions:
This protective effect may be associated with melatonin's both lipophilic and hydrophilic effects, thus providing on-site protection against free radical-mediated tissue damage.
To cite this abstract, please use the following information:
Acta Physiologica 2011; Volume 203, Supplement 686 :PC272