Melatonin the "light of night" in human biology and adolescent idiopathic scoliosis

The last decades melatonin has been used as a therapeutic chemical in a large spectrum of diseases, mainly in sleep disturbances and tumours and may play a role in the biologic regulation of mood, affective disorders, cardiovascular system, reproduction and aging. There are few papers regarding melatonin and its role in adolescent idiopathic scoliosis (AIS). Melatonin may play a role in the pathogenesis of scoliosis (neuroendocrine hypothesis) but at present, the data available cannot clearly support this hypothesis. Uncertainties and doubts still surround the role of melatonin in human physiology and pathophysiology and future research is needed.The biological pathway of melatonin is not simple. In the biosynthesis of melatonin, or N-acetyl-5-methoxytryptamine, tryptophan is first converted by tryptophan hydroxylase to 5-hydroxytryptophan, which is decarboxylated to serotonin (figure 1 and 2). The synthesis of melatonin from serotonin is catalyzed by two enzymes (arylalkylamine N-acetyltransferase and hydroxyindole-O-methyltransferase) (HIOMT) that are largely confined to the pineal gland [1,2]. Melatonin is rapidly metabolized, chiefly in the liver, by hydroxylation to 6-hydroxymelatonin. The urinary excretion of 6-sulfatoxymelatonin (the chief metabolite of melatonin) closely parallels serum melatonin concentrations [3].In humans melatonin is produced mainly in the pineal gland and a small portion in the retina. The synthesis and release of melatonin are stimulated by darkness, melatonin is the "chemical expression of darkness" and inhibited by light [4]. Photic information from the retina is transmitted to the pineal gland through the suprachiasmatic nucleus of the hypothalamus (SCN) and the sympathetic nervous system [5]. During daylight hours the retinal photoreceptor cells are hyperpolarized and inhibit the release of norepinephrine [6]. With the onset of darkness the photoreceptors release norepinephrine, thereby activating the system, and a number of a1- an