Abstract
Mitochondria play vital roles in metabolic energy transduction, intermediate molecule metabolism, metal ion homeostasis, programmed cell death and regulation of the production of reactive oxygen species. As a result of their broad range of functions, mitochondria have been strongly implicated in aging and longevity. Numerous studies show that aging and decreased lifespan are also associated with high reactive oxygen species production by mitochondria, increased mitochondrial DNA and protein damage, and with changes in the fatty acid composition of mitochondrial membranes. It is possible that the extent of fatty acid unsaturation of the mitochondrial membrane determines susceptibility to lipid oxidative damage and downstream protein and genome toxicity, thereby acting as a determinant of aging and lifespan. Reviewing the vast number of comparative studies on mitochondrial membrane composition, metabolism and lifespan reveals some evidence that lipid unsaturation ratios may correlate with lifespan. However, we caution against simply relating these two traits. They may be correlative but have no functional relation. We discuss an important methodology for body mass and phylogenetic correction in comparative studies.
Highlights
A brief history of longevity hypotheses Over a century ago, Max Rubner observed for six animal species that larger animals had a slower metabolic rate per unit mass and a longer lifespan compared with smaller animals
We suggest that empirical comparisons of membrane parameters for phylogenetically distant groups such as ectotherms and endotherms are complicated by differences in temperature regulation and weight-specific metabolism, which should be corrected for where possible
These studies were designed to identify the role of dietary polyunsaturated fatty acid (PUFA) on torpor patterns and hibernation, and revealed that dietary PUFAs led to a 7% increase in mitochondrial PUFA content and that these changes were paralleled by a 2.5°C decrease in minimum body temperature and longer torpor bouts [70,71]
Summary
A brief history of longevity hypotheses Over a century ago, Max Rubner observed for six animal species that larger animals had a slower metabolic rate per unit mass and a longer lifespan compared with smaller animals. These lipid peroxidation products result in membrane degeneration as well as protein and genome toxicity [56], culminating in aging and death (Figure 5) Such observations [27,49,50], led Pamplona and Barja to propose the homeoviscous-longevity adaptation hypothesis: namely, that the lower degree of fatty acid unsaturation in longevous animals decreases their sensitivity to lipid peroxidation and macromolecular damage. In pulse-label experiments of phosphatidylcholine and phosphatidylethanolamine, Schmid et al showed that only four fatty acid species were de novo synthesized (6:0–18:2 (n-6), 16:0–18:1, 16:0–22:6 (n-3) and 18:1–18:2 (n-6)), whilst the remainder were remodelled via rapid deacylation-reacylation [68] This may explain why in a recent phylogenomic study by Jobson [90] examining codon evolution across 25 mammalian species with different longevities, of genes with significantly high evolutionary selection in long-lived species there were a number of lipid membrane composition genes. Correlation being confused with causation without sufficient evidence or logical premise, or without due attention to confounding mechanisms, for example, polyunsaturated lipid peroxides causing aging rather than being associated with it for some other reason including physiological responses to stress
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