Role of the Antioxidant Activity of Melatonin in Myocardial Ischemia-Reperfusion Injury

Figures

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  Figure 1. Neural control of pineal melatonin synthesis and its physiological effects via receptors mediated and non-mediated actions (antioxidant activity). Daylight inhibits the pineal production of melatonin while darkness stimulates it. Melatonin acts in receptors MT 1 to 3. MT3 is important due to its antioxidative activities.

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  Figure 2. Pathophysiology of ischemia-reperfusion injury. The mechanisms through which myocardial tissue is damaged after the restoration of blood flow following a period of ischemia include oxidative stress, ion accumulation due to the dysfunction of cellular pumps, nitric oxide species that produce damage, mitochondrial dysfunction through the opening of MPTP and activation of cellular death pathways.

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  Figure 3. Mechanisms through which melatonin exerts myocardial protection in MI/R injury. Melatonin is capable of inhibiting the nitric oxide synthase, pro-inflammatory cytokines, ROS, and cellular pathways conducting to apoptosis. It is also responsible for enhancing anti-inflammatory mediators and antioxidant enzymes. Extracellularly, melatonin decreases atherosclerosis and improves dyslipidemias, which reduce the risk of ischemic episodes.