Abstract:
:Biochemical and structural changes occurring in the myocardium with aging are mainly resulting from the association of a general tissue atrophy with the hypertrophy of the remaining myocytes. Whilst hypertrophy seems to be a compensatory process to the loss of cardiomyocytes and to a mild systolic hypertensive condition that accompanies elderly people, atrophy should be the modification more closely related to aging 'per se.' In support to the free radical theory of aging, several signs of oxidative damage have been shown in the aged heart, such as lipofuscin accumulation, decreased phospholipid unsaturation index, greater formation of both hydrogen peroxide and 8-hydroxy-2'deoxyguanosine. As a compensatory reaction, the activities of the main oxygen-radical scavenger enzymes are stimulated in the mitochondria of aged rat heart. Endothelium-mediated vasoregulation is more susceptible to oxidative stress in aged with respect to young rats, suggesting that also the vasculature can be negatively influenced by the oxygen free radicals generated during aging. The possible primary role of oxygen free radicals in the development of myocardial atrophy is also discussed.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Muscari C,Giaccari A,Giordano E,Clô C,Guarnieri C,Caldarera CMdoi
10.1007/BF00240046subject
Has Abstractpub_date
1996-07-01 00:00:00pages
159-66eissn
0300-8177issn
1573-4919journal_volume
160-161pub_type
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