Mitochondrial DNA copy number and mitochondrial DNA deletion in adult and senescent rats
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2019, Environment InternationalCitation Excerpt :This may be explained by differences in the levels of fluoride exposure, nutritional status and population susceptibility. Mounting studies have showed that mtDNA encodes a variety of proteins, which is required for maintaining the normal function of mitochondria (Falkenberg et al., 2007; Malik and Czajka, 2013), while abnormal mtDNA results in mitochondrial dysfunction (Gadaleta et al., 1992; Malik et al. 2013). In addition, mtDNA are particularly sensitive to environmental factors because of their lack of repair capacity (Stewart and Chinnery, 2015).
Increased TFAM binding to mtDNA damage hot spots is associated with mtDNA loss in aged rat heart
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2016, NeuroToxicologyCitation Excerpt :Because cellular proliferation is an “energy-expensive” process and requires mitochondria capable of producing ATP, this could indicate one or more of the following regarding mitochondria in high passage DI-TNC1 astrocytes compared to their lower passage counterparts: (1) that there are fewer mitochondria overall, (2) that they contain the same number of mitochondria (or more), but there are fewer functional mitochondria in high passage DI-TNC1 astrocytes, or (3) that there are fewer mitochondria overall, and that they are less functional than in low passage DI-TNC1 astrocytes. It is most likely the second is true, as it has been shown that mitochondrial DNA (mtDNA) copy number increases with age in rodent brain (Gadaleta et al., 1992) (indicating the presence of more mitochondria overall), mitochondrial enzyme activity decreases in the aging brain (Leong et al., 1981), and mtDNA mutations increase (Corral-Debrinski et al., 1992), as does oxidative mtDNA damage (Mecocci et al., 1993). However, measures of mtDNA (copy number, mutations, and oxidative damage) and enzyme activity in whole regions of the brain are not necessarily reflective of what is occurring between and within cell types in those regions, and is likely differential between neurons and astrocytes.
Cardiac mitochondrial biogenesis in endotoxemia is not accompanied by mitochondrial function recovery
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