Abstract
To The Editor: For many years physiologists considered the pineal gland, lodged deep within the brain, a vestigial organ which was merely an anatomical remnant of a primary sensory system. However, over the past decade scientists have come to recognize melatonin, a product of the pineal gland, as a “master hormone” involved in the control of biological rhythms (Ebadi, 1984; Erlich & Apuzzo, 1985; Foley et al., 1986; Reiter, 1991) and more recently, it has been suggested that melatonin acts at a cellular level to regulate the genetic switching occurring in the cells throughout the body which promotes the aging process (Kloeden et al., 1990). Consequently, melatonin has been suspected as having anti-aging properties (Nair et al., 1986; Armstrong & Redman, 1991; Pierpaoli & Maestroni, 1987; Trentini et al., 1991) and the progressive decline in melatonin secretion with age (Nair et al., 1986; Sack et al., 1986; Thomas & Miles, 1989) led to the hypothesis that aging may be secondary to progressive pineal failure (Dilman et al., 1979; Reiter et al., 1980; Tang et al., 1985; Rozencwaig et al., 1987; Sandyk, 1990; Trentini et al., 1991; Grad & Rozencwaig, 1993). This hypothesis is supported by animal studies in which ablation of the pineal gland in rodents produces pathological changes resembling senescence which were reversed by the administration of a pineal extract or melatonin (Dilman et al., 1979; Armstrong & Redman, 1991). Moreover, senescence was delayed and life span prolonged when the pineal glands of young mice were grafted into old animals (Pierpaoli, 1991; Pierpaoli et al., 1991; Pierpaoli & Regelson, 1994).
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