الجذور الحرة المستحدثة بالإشعاع و أعراض الشيخوخة

Abstract EN

The universality of aging implies that its cause is basically the same in all species.

A free radical hypothesis of aging has been proposed that the free radicals produced during normal metabolism of the cell over time damage DNA and other macromolecules leading to degenerative diseases, malignancies, and eventual death of vital cells which in turn causes aging and death of the organism.

This hypothesis is supported by several observations.

Radiation produces its biologic effect through free radical formation and causes premature aging.

Second, the age pigment lipofuscin is associated with lipid peroxidation.

The hypothesis that oxygen radicals play a role in aging is also supported by the observation that, in general, long-lived species produce less endogenous free oxygen radicals because of their lower metabolic rate.

Long-lived animals also have more superoxide dismutase than do their short-lived counterparts, and animal species with the longest lifespan have the highest levels of superoxide dismutase.

Oxidative DNA damage is rapidly and effectively repaired.

It has been estimated that there are several thousand oxidative DNA damage sites in a human cell every day, and the majority of these are repaired.

However, a small fraction of unrepaired lesions could cause permanent changes in DNA and might be a major contributor to aging and cancer.

A consequence of the free radical hypothesis of aging is the idea that free radical scavenging agents might be used to prevent aging.