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Do Antioxidant Strategies Work against Aging and Age‐associated Disorders?

Identifieur interne : 003239 ( Main/Exploration ); précédent : 003238; suivant : 003240

Do Antioxidant Strategies Work against Aging and Age‐associated Disorders?

Auteurs : Kenichi Kitani [Japon] ; Chiyoko Minami [Japon] ; Takako Yamamoto [Japon] ; Wakako Maruyama [Japon] ; Setsuko Kanai [Japon] ; Gwen O. Ivy ; Maria-Cristina Carrillo [Argentine]

Source :

RBID : ISTEX:167EE84479A96406DAA5353AAB3C6DB7C497BEAB

English descriptors

Abstract

Abstract: The free radical theory of aging was initially proposed by Harman1 half a century ago primarily to explain biological aging processes. Although administration of so‐called antioxidant chemicals, which have been tested in the past for several decades, turned out to be mostly ineffective in prolonging the life spans of animals,2,3 the same theory of age‐associated diseases appears to be increasingly supported in the last two decades. Despite these difficulties, the success in extending life span of 4 different animal species (mice, rats, hamsters, and dogs) with (−)deprenyl (including a study of our group) indicates that there might exist another type of antioxidant strategy in addition to a simple administration of antioxidant chemicals (for review, see Refs. 4,5). (−)Deprenyl has also been shown to increase superoxide dismutase (SOD) and catalase (CAT) activities selectively in brain dopaminergic tissues.4,5 Interestingly, we have recently shown that another propargylamine, rasagiline not only increases antioxidant enzyme activities (CAT and SOD) in brain dopaminergic regions as (−)deprenyl does, but also increases CAT and SOD activities in extra‐brain catecholaminergic systems such as the heart and kidneys as well.6 These recent observations coupled with previous observations on the life span of animals with (−)deprenyl suggest that pharmacological modulation of endogenous antioxidant enzyme activities could be one potential antioxidant strategy against aging and age‐associated disorders. If the causal relationship between the two effects of (−)deprenyl exists as we hypothesized,4,5,7 we might be able to advance the elucidation of mechanism(s) of aging based on the free radical theory of aging.

Url:
DOI: 10.1111/j.1749-6632.2001.tb05654.x


Affiliations:


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<div type="abstract">Abstract: The free radical theory of aging was initially proposed by Harman1 half a century ago primarily to explain biological aging processes. Although administration of so‐called antioxidant chemicals, which have been tested in the past for several decades, turned out to be mostly ineffective in prolonging the life spans of animals,2,3 the same theory of age‐associated diseases appears to be increasingly supported in the last two decades. Despite these difficulties, the success in extending life span of 4 different animal species (mice, rats, hamsters, and dogs) with (−)deprenyl (including a study of our group) indicates that there might exist another type of antioxidant strategy in addition to a simple administration of antioxidant chemicals (for review, see Refs. 4,5). (−)Deprenyl has also been shown to increase superoxide dismutase (SOD) and catalase (CAT) activities selectively in brain dopaminergic tissues.4,5 Interestingly, we have recently shown that another propargylamine, rasagiline not only increases antioxidant enzyme activities (CAT and SOD) in brain dopaminergic regions as (−)deprenyl does, but also increases CAT and SOD activities in extra‐brain catecholaminergic systems such as the heart and kidneys as well.6 These recent observations coupled with previous observations on the life span of animals with (−)deprenyl suggest that pharmacological modulation of endogenous antioxidant enzyme activities could be one potential antioxidant strategy against aging and age‐associated disorders. If the causal relationship between the two effects of (−)deprenyl exists as we hypothesized,4,5,7 we might be able to advance the elucidation of mechanism(s) of aging based on the free radical theory of aging.</div>
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