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Fırat University Medical Journal of Health Sciences
2023, Cilt 37, Sayı 2, Sayfa(lar) 105-112
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The Effect of N-Acetylcysteine Administration on TRPM2 İon Channels in Aluminum Chloride-İnduced Cardiotoxic Rat Model
Sercan KAYA
The Effect of N-Acetylcysteine Administration on TRPM2 İon Channels in Aluminum Chloride-İnduced Cardiotoxic Rat Model
Keywords: Aluminum, cardiotoxicity, N-acetylcysteine, TRPM2

Objective: The heart is an important target organ for the accumulation of the biotoxic agent Aluminum (AL). This study aims to show whether the glutathione precursor N-acetylcysteine (NAC) has a cardioprotective effect against AL-induced cardiotoxicity and its effectiveness on the expression of transient receptor potential melastatin 2 (TRPM2) channels in a rat model.

Materials and Methods: Male Sprague-Dawley rats were randomly divided into 4 equal groups (n=7). No application was made to the control group. In the AL group, 30 mg/kg/day aluminum chloride was administered intraperitoneally (i.p.) for 14 days. The AL+NAC group was administered 150 mg/kg/day N-acetylcysteine i.p. for 14 days, 1 hour after aluminum chloride was administered i.p. at a dose of 30 mg/kg/day for 14 days. In the NAC group, 150 mg/kg/day N-acetylcysteine was administered, i.p. for 14 days. At the end of the 14th day, the rats were decapitated. After decapitation, heart tissues were removed and biochemical and histological analyzes were performed.

Results: Histopathological changes and increase in myocardial enzyme levels were observed in the AL group. It was observed that NAC application reduced AL-induced histopathological changes. In addition, it was determined that there was a significant increase in TRPM2 and Caspase 3 immunoreactivity in the AL group compared to the Control and NAC groups. In the AL+NAC group, there was a decrease in TRPM2 and Caspase 3 immunoreactivity compared to the AL group.

Conclusion: On AL-induced cardiotoxicity, NAC administration may exert a cardioprotective effect by reducing/attenuating biochemical and histopathological changes and regulating TRPM2 channel expression.


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