Heart cellular damaging effect

The cardioprotective effect of melatonin is demonstrated in several studies in in vivo and ex vivo experimental rat models or cardiomyocytes, as reviewed by Reiter.30 Melatonin administration in perfused rat hearts subjected to ischemia and reperfusion increased postischemic recovery of function, reduced the duration of ventricular tachycardia and ventricular fibrillation and this was associated with decreased lipid peroxidation products and OH radical formation, indicating an antioxidant effect of melatonin.31 Furthermore, in pinealectomized rats, occlusion of the left coronary artery followed by reperfusion resulted in significant increase in infarct size than in intact animals.32 Melatonin acts as scavenger of oxygen or nitrogen based reactants, stimulates antioxidant enzymes, stabilizes cellular membrane, increases the efficiency of oxidative phosphorylation, reduces leukocyte recruitment and adhesion molecule expression and reduces homocysteine induced damage (reviewed by Duncker33). 

Inflammation of blood vessel walls induces cellular proliferation, oxidation and deposition of cholesterol, and the development of atherosclerosis. These are ideal culture conditions for some tough bacteria, such as Chlamydia pneumoniae, which infect damaged arterial walls, and from their safe haven antagonize immune cells. Up to 80 per cent of people with cardiovascular disease are infected with Chlamydia, but whether this is a cause or an effect of heart disease is still disputed. It is simplest to say it could be both the cause of atherosclerosis is oxidative stress, and the process can be started, or perpetuated, by smoking, AGEs, oxidized cholesterol, ApoE4, infections, or just old age. Any one of these factors makes the others more likely. All are united by oxidative stress, and converted into the common currency of inflammation by NFkB and its kin. 

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