The origin of lipofuscin and possible consequences to the myocardium.
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.
D000328:Adult; D000368:Aged; D005260:Female; D006651:Histocytochemistry; D006801:Humans; D008062:Lipofuscin / Q000096:biosynthesis*; D008247:Lysosomes / Q000378:metabolism; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D008875:Middle Aged; D008929:Mitochondria, Heart / Q000378:metabolism / Q000648:ultrastructure; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D010860:Pigments, Biological / Q000096:biosynthesis*
D008062:Lipofuscin; D010860:Pigments, Biological; D008315:Malondialdehyde