Kloeden P E, Rössler R, Rössler O E
Medical Policlinic, University of Tübingen, Germany.
Exp Gerontol. 1993 Mar-Apr;28(2):109-18. doi: 10.1016/0531-5565(93)90001-t.
Genetically programmed aging, with its cellular genetic switching implied by the in vitro Hayflick limit, requires additional timing devices to coordinate the switching processes within the different cells of a highly complex life form. Evolutionary arguments have been presented elsewhere to support the need for a centralized timing mechanism as against a localized mean-field alternative. Extensive evidence is now available for the role of the pineal gland and its secreted melatonin in the aging process. The nightly melatonin peak changes with age, thus providing a potential signal to inform all of the cells in the organism of its age. Here it is hypothesized that the decoding of this "durational signal" at the cellular level is carried out with the aid of the sleep induced pCO2 changes in the blood. To test this hypothesis, modifications of the in vitro Hayflick experiment and of the in vivo Pierpaoli longevity experiment involving rhythmic addition of melatonin and pH manipulations are proposed.
基因编程衰老，体外海弗利克极限暗示其存在细胞遗传开关，这需要额外的计时装置来协调高度复杂生命形式中不同细胞内的开关过程。其他地方已经提出了进化论观点来支持需要一种集中计时机制而非局部平均场替代方案。现在有大量证据表明松果体及其分泌的褪黑素在衰老过程中的作用。夜间褪黑素峰值随年龄变化，从而为告知生物体所有细胞其年龄提供了一个潜在信号。在此假设，这种“持续时间信号”在细胞水平上的解码是借助睡眠诱导的血液中二氧化碳分压变化来进行的。为了验证这一假设，建议对体外海弗利克实验和体内皮尔帕奥利长寿实验进行修改，包括有节律地添加褪黑素和进行酸碱度操作。
