After a rapid examination of a few basic concepts concerning cellular aging and programmed cell death, the aging of the tissues and organs, the authors discuss the principal theories on senescence. They underline that it is necessary to agree in considering the various genetic and epigenetic, endogenous and exogenous mechanisms that lead to the complex aging phenomenon multiple and interrelated. In particular they stress the hypothesis that senescence can be due to a sum of molecular damages caused by free radicals, and to the loss of telomeric DNA. Radical reactions can cause mutations, inactivation or a decrease in the turnover of mitochondrial DNA which is more vulnerable than the nuclear genoma to the attack of mutagenic agents, acting also as a continuous source of initial and/or promoting factors of the carcinogenetic process. The somatic cells become senescent because during cell division, they lose the mechanisms for the lengthening of the telomere. The telomerase prevents the shortening of telomeres in neoplastic cells and therefore renders them immortal. Paradoxically the protection of the telomere is exactly what must be avoided in the case of tumor cells. Recently the demonstration that telomerase is not always involved in the restoration of telomere length shows the complexity of the problems connected to the cause of senescence.