Koobs D H, Schultz R L, Jutzy R V
Arch Pathol Lab Med. 1978 Feb;102(2):66-8.
Examination by light and electron microscopy of human myocardium from necropsies and biopsy specimens has revealed evidence that mitochondria can be transformed into granules of lipofuscin. This pigment has been shown to arise from peroxidative destruction of polyunsaturated lipid membranes. A high rate of lipofuscin formation is indicated by the occurrence of brown atrophy of the heart in relatively young persons who died of conditions that were associated with inanition. Such lipofuscin formation suggests the importance of dietary antioxidants in preventing peroxidative damage to mitochondria. A by-product of lipid peroxidation, malonaldehyde, can react with nuclear DNA, blocking template activity. Nuclear damage of this kind could reduce the capacity for protein synthesis and limit mitochondrial and contractile protein replacement. Such a limitation would contribute to heart failure during stress. Peroxidative damage to the myocardium is cumulative and irreversible.
通过对尸检和活检标本中的人体心肌进行光学显微镜和电子显微镜检查发现，有证据表明线粒体可转化为脂褐素颗粒。这种色素已被证明是由多不饱和脂质膜的过氧化破坏产生的。在死于与营养不良相关疾病的相对年轻的人身上出现心脏褐色萎缩，表明脂褐素形成率很高。这种脂褐素的形成表明饮食中的抗氧化剂在预防线粒体过氧化损伤方面的重要性。脂质过氧化的副产物丙二醛可与核DNA反应，阻断模板活性。这种核损伤会降低蛋白质合成能力，并限制线粒体和收缩蛋白的替换。这种限制会导致应激期间的心力衰竭。心肌的过氧化损伤是累积性的且不可逆的。
