Abstract

Phagocytosis is an important element of the nonspecific immune response because it is a fundamental mechanism of defense against infectious agents. Phagocytic cells first ingest the target (antigen) and then destroy it by the action of enzymes by means of a series of redox reactions known as the respiratory burst. In this process, several aggressive chemical species are formed, including superoxide anion, hydrogen peroxide, the hydroxyl radical, and hypochlorite to destroy the invasive microorganisms. Once their work is done, the free radicals are scavenged or eliminated by the antioxidant mechanisms that the phagocytes have available, thereby ensuring the integrity of these cells. The effect of melatonin on phagocytosis has been studied in depth. Melatonin at pharmacological concentrations increases both the chemoattractive capacity (chemotaxis) of these cells and their capacity to phagocytose antigen particles and reduces the intensity of the respiratory burst. The changes in plasma melatonin levels were found to be positively correlated with phagocytosis and negatively with the oxidative metabolism. Studies showed daily oscillations of the levels of this hormone in young animals and a decline in plasma levels with advancing age. The decline is accompanied by a loss of the daily rhythm, with no significant differences being found between nocturnal and diurnal values in old animals. Given that melatonin acts by sending information to the organism on its temporal organization, this hormone could be an important pharmacological agent for the attenuation of age-related changes in the immune system, circadian organization, sleep, and other disorders accompanying old age.

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