MtDNA Deletions in Aging and in Nonmitochondrial Pathologies

Cormio, Antonella; Lezza, Angela Maria Serena; Vecchiet, Jacopo; Felzani, Giorgio; Marangi, L.; Guglielmi, Francesco William; Francavilla, A.; Cantatore, Palmiro; Gadaleta, Maria Nicola

doi:10.1111/j.1749-6632.2000.tb06658.x

Cited by 9 publications

(2 citation statements)

References 4 publications

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“…Several human studies analysing postmortem brain tissue have confirmed that mutations, such as the 4977-kb deletion, 7436-kb deletion, and 8-oxodG accumulate with age (Cortopassi & Arnheim 1990, Corral-Debrinski et al 1992a, Blanchard et al 1993). Mitochondrial deletions have been discussed in depth in several excellent articles (Cortopassi & Arnheim 1990, Wallace 1997, Gadaleta et al 1998, Cormio et al 2000. Mitochondrial deletions have been discussed in depth in several excellent articles (Cortopassi & Arnheim 1990, Wallace 1997, Gadaleta et al 1998, Cormio et al 2000.…”

Section: Oxidant Production In Proximity Of Mtdnamentioning

confidence: 99%

“…There may exist regional variations in the accretion of mtDNA mutations, as the cortex and putamen of aged human brains showed increased levels of the 4977-kb common deletion but the cerebellum did not (Corral-Debrinski et al 1992a). Mitochondrial deletions have been discussed in depth in several excellent articles (Cortopassi & Arnheim 1990, Wallace 1997, Gadaleta et al 1998, Cormio et al 2000.…”

Section: Oxidant Production In Proximity Of Mtdnamentioning

confidence: 99%

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Ageing and subcellular distribution of mitochondria: role of mitochondrial DNA deletions and energy production

Drew¹,

Leeuwenburgh²

2004

Acta Physiologica Scandinavica

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The rapid growing population of elderly illustrates the importance of understanding the mechanisms responsible for ageing and the detrimental effects on health associated with increasing age. One of the primary mechanisms may be because of the accumulation of mtDNA damage and oxidative damage with age. Previous studies have examined this correlation in post-mitotic tissues such as skeletal muscle, heart and brain with decreased mitochondrial function, such as enzymatic activities of the electron transport chain and ATP production. However, regional differences in the subcellular location of mitochondria exist and most studies have failed to differentiate the effects of these two autonomous fractions, the subsarcolemmal and intermyofibrillar populations. Hence, while future research attempts to explain the mechanisms responsible for ageing in the mitochondrion, it should also take into account the independent pathways of these two distinctly different populations.

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