Genetic and functional changes in mitochondria associated with aging

Ozawa, Takayuki

doi:10.1152/physrev.1997.77.2.425

Cited by 282 publications

(173 citation statements)

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“…The mitochondrial genome is extremely susceptible to damages from continuous exposure to ROS. These molecules endogenously are produced in mitochondrial respiratory chain and are evidenced to increase the ratio of point mutations in mtDNA [47]. This effect is probably through inhibition of the repair system in mtDNA, detoxification of ROS, or Due to difficulties for obtaining aborted materials, our work was only focused on maternal blood.…”

Section: Discussionmentioning

confidence: 99%

No mitochondrial DNA deletions but more D-loop point mutations in repeated pregnancy loss

Seyedhassani

Houshmand

Kalantar

et al. 2010

J Assist Reprod Genet

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Purpose Repeated pregnancy loss (RPL) occurs in 1 out of 300 couples, and the cause of about 50% of them remains idiopathic. Mitochondria have an important role in human development through ATP production and their involvement in apoptosis. Methods 96 RPL and 96 control females were used to investigate the frequency of deletions and point mutations in the displacement loop (D-loop) on mitochondria. Multiplex PCR and DNA sequencing methods were used to detect possible variations in the mitochondrial DNA (mtDNA).Results No deletions but a high frequency of point mutations were found in RPL females; among 129 variations observed in RPL, 22 mutations were significant (P<0.05) and the insertion of C in nucleotide 114 was novel. Conclusion High rate of mutations in D-loop of mtDNA was observed in maternal blood, a fact that may have a direct or indirect role in inducing RPL. The results can be used in the assessment of RPL and designing possible treatments for improving assisted reproduction.

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Section: Discussionmentioning

confidence: 99%

No mitochondrial DNA deletions but more D-loop point mutations in repeated pregnancy loss

Seyedhassani

Houshmand

Kalantar

et al. 2010

J Assist Reprod Genet

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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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“…They are often enlarged, sometimes excessively, and thus are called 'giant' mitochondria [54,55]. Mutations of mtDNA and protein alterations steadily increase with age [57,58]. The proportion of normal mitochondria progressively declines, resulting in diminished respiration and lowered ATP production [54,56].…”

Section: Cellular Manifestations Of Ageingmentioning

confidence: 99%

“…Thus, mitochondria represent the primary target of self-produced ROS, probably explaining why these organelles are particularly affected by age. Another probable reason for the pronounced changes of mitochondria in ageing cells follows from the properties of mtDNA, which lacks introns, is almost completely expressed, and has a relatively low repair capacity [57]. Mutations of mtDNA can account for the defective synthesis of 13 respiratory chain proteins, while alterations to other proteins would reflect damage to nDNA.…”

Section: Mechanisms Of Mitochondrial Damagementioning

confidence: 99%

Autophagy, organelles and ageing

Terman

Gustafsson

Brunk

2007

The Journal of Pathology

263

210

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As a result of insufficient digestion of oxidatively damaged macromolecules and organelles by autophagy and other degradative systems, long-lived postmitotic cells, such as cardiac myocytes, neurons and retinal pigment epithelial cells, progressively accumulate biological 'garbage' ('waste' materials). The latter include lipofuscin (a non-degradable intralysosomal polymeric substance), defective mitochondria and other organelles, and aberrant proteins, often forming aggregates (aggresomes). An interaction between senescent lipofuscin-loaded lysosomes and mitochondria seems to play a pivotal role in the progress of cellular ageing. Lipofuscin deposition hampers autophagic mitochondrial turnover, promoting the accumulation of senescent mitochondria, which are deficient in ATP production but produce increased amounts of reactive oxygen species. Increased oxidative stress, in turn, further enhances damage to both mitochondria and lysosomes, thus diminishing adaptability, triggering mitochondrial and lysosomal pro-apoptotic pathways, and culminating in cell death.

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Genetic and functional changes in mitochondria associated with aging

Cited by 282 publications

References 0 publications

No mitochondrial DNA deletions but more D-loop point mutations in repeated pregnancy loss

No mitochondrial DNA deletions but more D-loop point mutations in repeated pregnancy loss

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

Autophagy, organelles and ageing

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