Reduced Mitochondrial DNA Transcription in Senescent Rat Heart

Andreu, Antoni L.; Arbós, M.A.; Pérez‐Martos, Acisclo; López‐Pérez, Manuel J.; Asín, J. A. Casas; López, Natalia Barrios; Montoya, Julio; Schwartz, S.

doi:10.1006/bbrc.1998.9703

Cited by 40 publications

(24 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The study performed by Andreu et al [62] showed an age-related reduction in newly-synthesized mitochondrial RNAs that reflects a decrease in the synthesis rate. The authors also reported an age-related increase in protein carbonyl content of the mitochondrial membranes, suggesting an accumulation of mitochondrial oxidative damage in senescent mitochondria.…”

Section: Discussionmentioning

confidence: 98%

Inhibition of Mitochondrial Respiratory Chain in the Brain of Adult Rats After Acute and Chronic Administration of Methylphenidate

et al. 2009

View full text Add to dashboard Cite

Methylphenidate (MPH) is frequently prescribed for the treatment of attention deficit/hyperactivity disorder. It was previously demonstrated that MPH altered brain metabolic activity. Most cell energy is obtained through oxidative phosphorylation, in the mitochondrial respiratory chain. However, there are still few studies about MPH effects on the brain of adult rats. Thus, in the present study we evaluated the effect of acute or chronic administration of MPH on the activities of mitochondrial respiratory chain complexes I-IV in the brain of adult rats. For acute administration, a single injection of MPH was given to 60-day-old rats. For chronic administration, MPH injections were given to 60-day-old rats once daily for 28 days. Our results showed that complexes I, II, III and IV were inhibited after acute or chronic MPH administration in the hippocampus, prefrontal cortex, striatum and cerebral cortex. On the other hand, cerebellum was not affected.

show abstract

Section: Discussionmentioning

confidence: 98%

Inhibition of Mitochondrial Respiratory Chain in the Brain of Adult Rats After Acute and Chronic Administration of Methylphenidate

et al. 2009

View full text Add to dashboard Cite

show abstract

“…Of the five respiratory chain complexes, Complex I (NADH-ubiquinone reductase or NADH dehydrogenase) appears to be the most susceptible to age-related declines in activity (3,16,72,122,126), although some studies have reported no significant changes in Complex I activity with age (63,81). Physiologically relevant ROS generation occurs at the flavin mononucleotide group (FMN) of complex I through reversed electron transfer using complex II substrate succinate (77).…”

Section: Age-related Alterations In Cardiac Mitochondrial Functionmentioning

confidence: 99%

“…Given that 7 of the 13 mtDNA encoded polypeptides in the respiratory chain complex are found in complex I, it is not surprising that this complex would be most greatly affected with aging if the mitochondrial theory of aging proves to be true (72). In addition, many studies report age-associated declines in the activities of complex III (ubiquinol-cytochrome c reductase) (16,74) and complex IV (cytochrome c oxidase) (3,16,27,63,122), which also contain mtDNA encoded proteins, while the activity of complex II (succinate dehydrogenase) appears unaffected (81,122,126) or even increased (16,63). This finding is noteworthy, since mtDNA does not encode for any of the polypeptides in complex II (92).…”

Section: Age-related Alterations In Cardiac Mitochondrial Functionmentioning

confidence: 99%

Cardiac mitochondrial bioenergetics, oxidative stress, and aging

Judge¹,

Leeuwenburgh²

2007

American Journal of Physiology-Cell Physiology

125

View full text Add to dashboard Cite

Mitochondria have been a central focus of several theories of aging as a result of their critical role in bioenergetics, oxidant production, and regulation of cell death. A decline in cardiac mitochondrial function coupled with the accumulation of oxidative damage to macromolecules may be causal to the decline in cardiac performance with age. In contrast, regular physical activity and lifelong caloric restriction can prevent oxidative stress, delay the onset of morbidity, increase life span, and reduce the risk of developing several pathological conditions. The health benefits of life long exercise and caloric restriction may be, at least partially, due to a reduction in the chronic amount of mitochondrial oxidant production. In addition, the available data suggest that chronic exercise may serve to enhance antioxidant enzyme activities, and augment certain repair/removal pathways, thereby reducing the amount of oxidative tissue damage. However, the characterization of age-related changes to cardiac mitochondria has been complicated by the fact that two distinct populations of mitochondria exist in the myocardium: subsarcolemmal mitochondria and interfibrillar mitochondria. Several studies now suggest the importance of studying both mitochondrial populations when attempting to elucidate the contribution of mitochondrial dysfunction to myocardial aging. The role that mitochondrial dysfunction and oxidative stress play in contributing to cardiac aging will be discussed along with the use of lifelong exercise and calorie restriction as countermeasures to aging.

show abstract

“…Some laboratories report no attenuation of respiratory complexes with age (Torii et al, 1992;Barazzoni et al, 2000;Kwong & Sohal, 2000), whereas others have observed decreased complex I and IV activities (Sugiyama et al, 1993;Andreu et al, 1998), transcript levels (Andreu et al, 1998;Hudson et al, 1998) and protein synthesis (Hudson et al, 1998). In rat models of congestive heart failure, declines in transcripts for subunits of complex IV and enzyme activity are associated with decreased levels of the nuclear factors PGC-1α, Tfam and NRF-2 (Garnier et al, 2003).…”

Section: (Ii) Heartmentioning

confidence: 99%

Is defective electron transport at the hub of aging?

Maklashina

Ackrell

2003

Aging Cell

View full text Add to dashboard Cite

SummaryThe bulwark of the mitochondrial theory of aging is that a defective respiratory chain initiates the death cascade. The increased production of superoxide is suggested to result in progressive oxidant damage to cellular components and particularly to mtDNA that encodes subunits assembled in respiratory complexes. Earlier studies of respiration in muscle mitochondria obtained from large cohorts of patients supported this notion by showing that either singly or in combinations, the respiratory complexes exhibited decreased activity in the elderly. The following critique of the most cited publications over the past decade points out the systematic errors that put earlier work at odds with recent findings. These later investigations indicate that aging has no overt effect on either the electron transport system or oxidative phosphorylation.

show abstract

Reduced Mitochondrial DNA Transcription in Senescent Rat Heart

Cited by 40 publications

References 30 publications

Inhibition of Mitochondrial Respiratory Chain in the Brain of Adult Rats After Acute and Chronic Administration of Methylphenidate

Inhibition of Mitochondrial Respiratory Chain in the Brain of Adult Rats After Acute and Chronic Administration of Methylphenidate

Cardiac mitochondrial bioenergetics, oxidative stress, and aging

Is defective electron transport at the hub of aging?

Contact Info

Product

Resources

About