Muscari C, Giaccari A, Giordano E, Clô C, Guarnieri C, Caldarera C M
Department of Biochemistry G. Moruzzi, University of Bologna, Italy.
Mol Cell Biochem. 1996 Jul-Aug;160-161:159-66. doi: 10.1007/BF00240046.
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.
随着年龄增长，心肌中发生的生化和结构变化主要是由于一般组织萎缩与剩余心肌细胞肥大共同作用的结果。虽然肥大似乎是对心肌细胞丧失以及老年人伴随的轻度收缩期高血压状态的一种代偿过程，但萎缩应该是与衰老“本身”更密切相关的改变。为支持衰老的自由基理论，在老年心脏中已显示出氧化损伤的若干迹象，如脂褐素积累、磷脂不饱和指数降低、过氧化氢和8 - 羟基 - 2'-脱氧鸟苷生成增多。作为一种代偿反应，老年大鼠心脏线粒体中主要氧自由基清除酶的活性受到刺激。与年轻大鼠相比，老年大鼠的内皮介导的血管调节对氧化应激更敏感，这表明衰老过程中产生的氧自由基也可能对血管系统产生负面影响。本文还讨论了氧自由基在心肌萎缩发展过程中可能的主要作用。
