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

Abstract

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.

A comparative analysis of the cell biology of senescence and aging

“…This may relate to the significantly decreased rate of mitochondrial biogenesis in combination with an accumulation of defective mtDNA [169]. Large-scale deletion of mtDNA is a well-characterized change occurring in cells from old animals [170]. These deletions frequently correlate with abnormal electron transport chain activity (hypoactivity of cytochrome c oxidase and hyperactivity of succinate dehydrogenase) and are blamed as a contributing factor for age-related sarcopenia [171].…”

Exercise in a hot environment influences plasma anti-inflammatory and antioxidant status in well-trained athletes

“…heat cramps, heat exhaustion, heat stroke) and/or accidents if left unchecked (Wright et al, 2014). Body temperature affects leukocyte mobilization, cytokines and markers of neutrophil activation during and after exercise, resulting in a systemic activation in a hot environment (Drew and Leeuwenburgh, 2004;Mestre-Alfaro et al, 2012). Hyperthermia has been shown to increase exercise-induced oxidative stress and to selectively affect specific lipid oxidation markers such as F 2 -isoprostanes (Dieing et al, 2003).…”

Acute and long-term effects of botulinum neurotoxin on the function and structure of developing extraocular muscles

“…Mitochondria are sensitive markers for the functional state of muscles (Capetanaki, 2002;Drew and Leeuwenburgh, 2004;Fluck and Hoppeler, 2003;Hoppeler et al, 1987). Mitochondria respond to BoNT treatment in adult mammalian extraocular muscles with significant morphological alterations (Spencer and McNeer, 1987).…”

“…Mitochondria are sensitive markers for the functional state of muscles (Capetanaki, 2002;Drew and Leeuwenburgh, 2004;Fluck and Hoppeler, 2003), and BoNT treatment in adult and juvenile mammalian EOMs has significant effects on mitochondria, particularly in the acute phase of paralysis (Spencer, 1987;Spencer et al, 1992). Therefore, we paid particular attention to the acute and long-term effects of BoNT treatment on quantitative and spatial aspects of mitochondria in developing chicken EOMs.…”