The Effect of Age on Mitochondrial Ultrastructure

Wilson, Patricia D.; Franks, L. M.

doi:10.1159/000212035

Cited by 80 publications

(27 citation statements)

References 8 publications

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“…Mitochondria appear to generally decrease in number and size as a function of aging; the smallest mitochondria with shortest cristae were observed in the oldest rats (5,7). Similar observations have been documented in both mice and humans (7,10,11). Overall mitochondrial phosphorylation as well as turnover of mitochondrial proteins are reduced in the aged liver (7,12).…”

supporting

confidence: 82%

Biology of senescent liver peroxisomes: role in hepatocellular aging and disease.

Youssef

Badr

1999

Environ Health Perspect

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Despite rising interest in the health problems of the elderly, information on senescence-related alterations in essential metabolic pathways and their responses to various chemicals is scarce. Although peroxisomal pathways are involved in a multitude of cellular fnctions, little attention has been given to the potential relationship between senescence of these organelles and the process of aging and disease. Although the prevailing experimental evidence points to a decline in liver peroxisomal enzyme activities and a muted response to peroxisome-proleratn chemicals in aged animals, it is also evident that aged animals are more susceptible, inl comparison to their young counterparts, to the hepatocarcinogenic efecs of these chemicals. Furthermore, little is known about extraperoxisomal effects of peroxisome proliferators in aged animals. This review evaluates published studies on the impat of aging on basal hepatic:peroxisomal metabolism, response to peroxisome proliferators, and changes in signal trauction pathways involved in these processes, with the aim of stimulating research efforts in this important area. The potential intricate relationship among senescent perosomes, aged hepatocytes, and health are also discussed.

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supporting

confidence: 82%

Biology of senescent liver peroxisomes: role in hepatocellular aging and disease.

Youssef

Badr

1999

Environ Health Perspect

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“…Since mitochondria did not appear swollen in any age group, this finding indicates that mitochondria increase in size with age. Age-related increases in mitochondrial size have been reported in the rat cerebellum [2] and in human [24] and mouse [28] liver (for review see [18]); however, Herbener [7] found no such changes in mouse heart and liver.…”

Section: Discussionmentioning

confidence: 99%

Age-related quantitative changes in mitochondria of satellite cell sheaths enveloping spinal ganglion neurons in the rabbit

Martinelli

Sartori

Ledda

et al. 2003

Brain Research Bulletin

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We studied mitochondria in the satellite cell sheaths which envelope the spinal ganglion neurons of rabbits aged 12, 42, and 79 months. While the mean cytoplasmic volume of satellite cell sheaths did not change significantly with age, the mean percentage of cytoplasmic volume occupied by mitochondria decreased with age. This decrease is mainly due to a reduction in the total mitochondrial mass and only in minor part is a consequence of lipofuscin accumulation. Mitochondrial structure did not change, while mitochondrial size increased with age. Comparison between mitochondria in nerve cell bodies and those in satellite cell sheaths showed that: (1) the mean percentage of cytoplasmic volume occupied by mitochondria was greater in nerve cell bodies than satellite cell sheaths and the ratio between these two percentages remained constant with advancing age; (2) the total mitochondrial mass was much greater in nerve cell bodies than satellite cell sheaths and the ratio between these two values increased with age; (3) the extent of increase of mitochondrial size with age was similar in nerve cell bodies and satellite cell sheaths. The results of the present study suggest that: (1) the ability of satellite cell sheaths to produce energy decreases with age; (2) the decreased ability of sensory neurons in old animals to meet high energy demands may be partly due to the diminished contribution of their associated satellite cell sheaths.

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“…Studies of the effects of aging on mitochondria have shown defects in ultrastructure, 22 decreased electron transport chain activity. 23 decreased activity of individual electron chain complexes, 24,25 mitochondria DNA 26 and mitochondrial transcription.…”

Section: Agingmentioning

confidence: 99%

Indirect measurement of mitochondrial proton leak and its application

et al. 1999

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In mitochondria, ATP synthesis is coupled to oxygen consumption by the proton electrochemical gradient established across the mitochondrial inner membrane in a process termed oxidative phosphorylation. It has long been known from stoichiometric studies that ATP synthesis is not perfectly coupled to oxygen consumption. The major inef®ciency in the system is leakage of protons across the mitochondrial inner membrane driven by the proton electrochemical gradient. The kinetics of the proton leak can be determined indirectly, by measuring the oxygen consumption of mitochondria under non-phosphorylating conditions (plus oligomycin) as a function of the proton electrochemical gradient. This experimental system provides a convenient means to investigate inner membrane permeability to protons and the effect of factors that may effect that permeability. In this paper we review some results from our laboratory of indirect measurement of mitochondrial proton leak and how it has been applied to investigate the effect of aging, obesity and thyroid status on proton leak. The results show that (i) proton leak in isolated liver mitochondria is not signi®cantly different in a comparison of young and old rats, in contrast (ii) there is an apparent increase in proton leak in in situ mitochondria in hepatocytes from old rats when compared to those from young rats, (iii) proton leak in neuronal mitochondria in situ in synaptosomes is not signi®cantly different in young and old rats, (iv) proton leak is greater in isolated liver mitochondria from obaob mice compared to lean controls, (v) acute leptin (OB protein) administration restores the increased leak rate in isolated liver mitochondria from obaob mice to that of lean controls, (vi) administration of thyroid hormone (T 3 ) increases proton leak in rat muscle mitochondria, and (vii) proton leak in muscle mitochondria is insensitive to the presence of GDP. It is proposed that the experimental system described here for measuring proton leak, is an ideal functional assay for determining whether the novel uncoupling proteins increase inner membrane permeability to protons.

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The Effect of Age on Mitochondrial Ultrastructure

Cited by 80 publications

References 8 publications

Biology of senescent liver peroxisomes: role in hepatocellular aging and disease.

Biology of senescent liver peroxisomes: role in hepatocellular aging and disease.

Age-related quantitative changes in mitochondria of satellite cell sheaths enveloping spinal ganglion neurons in the rabbit

Indirect measurement of mitochondrial proton leak and its application

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