Mitochondrial theory of aging : to be or not to be ? (The role of Linoleic acid)
The use of linoleic acid based on its interaction on the mitochondria to increase maximum lifespan is first suggested More
After years of frustration over his inability to increase maximum lifespan with antioxidant supplements, Harman came to the conclusion that mitochondria were producing as well as being damaged by free radicals, but that exogenous antioxidants don't enter the mitochondria. And that it is mitochondria that determine lifespan.
Linoleic acid (LA) improves insulin resistance and prevents diabetes.
Linoleic acid protects RPT (renal proximal tubules ) during the late phase of cell death associated with inhibition of the electron transport chain but not oxidative injury.
Aging results in a redistribution of polyunsaturated fatty acids (PUFAs) in myocardial phospholipids. In particular, a selective loss of linoleic acid (18:2n6) with reciprocal increases of long-chain PUFAs (eg, arachidonic and docosahexaenoic acids) in the mitochondrial phospholipid cardiolipin correlates with cardiac mitochondrial dysfunction and contractile impairment in aging and related pathologies.
A significant allometric increase in linoleic acid (C18:2 n6) (r=0.986), polyunsaturated (r=0.990) and UI (r=0.904) was observed in the larger birds. Birds are unique since they can combine a high rate of oxygen consumption at rest with a high maximum life span (MLSP).
Patterns of age-related changes in ad libitum (AL) fed rats: membrane levels of long-chain polyunsaturated fatty acids, 22:4 and 22:5, increased progressively, while membrane linoleic acid (18:2) decreased steadily with age.
The use of linoleic acid based on its interaction on the mitochondria to increase maximum lifespan is first suggested.
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