Mitochondrial enzyme activities as biochemical markers of aging

Navarro, Ana

doi:10.1016/j.mam.2004.02.007

Cited by 77 publications

(40 citation statements)

References 55 publications

(62 reference statements)

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“…These observations are consistent with previous reports that ATP synthase activity decreases with advancing age in the erythrocytes of cows (Bartosz et al 1982) and the hearts of mice (Yarian et al 2005). Similarly, NADH dehydrogenase activity has also been reported to decrease with advancing age in the kidneys, livers, and testes of rats (Napoleone et al 1991;Torres-Mendoza et al 1999;Vázquez-Memije et al 2008), as well as in the livers and brains of mice (Navarro et al 2002;Navarro 2004).…”

Section: δψMsupporting

confidence: 92%

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Chuang

Hsu

2012

AGE

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Trophocytes and fat cells in honeybees (Apis mellifera) have served as targets for cellular senescence studies, but mitochondrial energy utilization with advancing age in workers is unknown. In this study, mitochondrial energy utilization was evaluated in the trophocytes and fat cells of young and old workers reared in a field hive. The results showed that (1) mitochondrial density increased with advancing age; (2) mitochondrial membrane potential (ΔΨm), nicotinamide adenine dinucleotide oxidized form (NAD + ) concentration, adenosine triphosphate (ATP) concentration, and NAD + /nicotinamide adenine dinucleotide reduced form (NADH) ratio decreased with advancing age; and (3) the expression of NADH dehydrogenase 1 (ND1), ATP synthase, and voltage-dependent anion channel 1 (VDAC1) increased with advancing age, whereas ND1 and ATP synthase did not differ with advancing age after normalization to mitochondrial density and VDAC1. These results show that the trophocytes and fat cells of young workers have higher mitochondrial energy utilization efficiency than those of old workers and that aging results in a decline in mitochondrial energy utilization in the trophocytes and fat cells of worker honeybees.

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Section: δψMsupporting

confidence: 92%

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Chuang

Hsu

2012

AGE

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“…While the mtDNA/mitochondrion ratio is essentially constant in all cell types in mammalian species, the number of mitochondria per cell and the amount of mtDNA per cell seem to be closely regulated within a given cell type but differ widely between cell types (Robin & Wong, 1988). Total mitochondrial gene expression seems to be a direct function of ageing, and generally declines with age, as has been demonstrated in a number of studies (Bodyak et al, 2002 ;Lu et al, 2004), while the activity of mitochondrial enzymes is suggested as a biochemical marker of ageing (Navarro et al, 2004). Importantly, ageing might affect the expression of individual mitochondrial genes to various extents (Tollet-Egnell et al, 2001).…”

Section: Discussionmentioning

confidence: 87%

A large-scale screening of the normalized mammalian mitochondrial gene expression profiles

Anisimov

2005

Genet. Res.

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SummaryMammalian mitochondrial genomes are organized in a conserved and extremely compact manner, encoding molecules that play a vital role in oxidative phosphorylation (OXPHOS) and carry out a number of other important biological functions. A large-scale screening of the normalized mitochondrial gene expression profiles generated from publicly available mammalian serial analysis of gene expression (SAGE) datasets (over 17 . 7 millions of tags) was performed in this study. Acquired SAGE libraries represent an extensive range of human, mouse, rat, bovine and swine cell and tissue samples (normal and pathological) in a variety of conditions. Using a straightforward in silico algorithm, variations in total mitochondrial gene expression, as well as in the expression of individual genes encoded by mitochondrial genomes are addressed, and common patterns in the species-and tissue-specific mitochondrial gene expression profiles are discussed.

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“…Finally, all three subunits are essential for the formation of an active, stable complex: a knock-out of a single subunit produces a functional knock-out of the entire enzyme (Dyck et al, 1996;Woods et al, 1996;Pan and Hardie, 2002 (Hardie et al, 2003;Dasgupta and Milbrandt, 2007) suggests possible involvement of this enzyme in neuroprotective processes. Furthermore, in the nervous system, as in most other tissues, normal aging is associated with increased amounts of oxidative stress and perturbed cellular energy metabolism involving impaired efficiency of mitochondrial ATP production (Floyd and Hensley, 2002;Navarro, 2004). Therefore, one can imagine that the need for a functional metabolic sensor increases during aging.…”

Section: Discussionmentioning

confidence: 99%

Drosophila alicorn Is a Neuronal Maintenance Factor Protecting against Activity-Induced Retinal Degeneration

Spasic¹,

Callaerts²,

Norga³

2008

Journal of Neuroscience

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Exploring mechanisms that govern neuronal responses to metabolic stress is essential for the development of therapeutic strategies aimed at treatment of neuronal injury and disease. AMP-activated protein kinase (AMPK) is a key enzyme regulating cellular energy homeostasis that responds to changes in cellular energy levels by promoting energy-restorative and inhibiting energy-consumptive processes. Recent studies have suggested that AMPK might have a neuroprotective function. However, the existing evidence is contradictory and almost exclusively derived from in vitro studies based on drug treatments and metabolic stress models. To tackle these issues in vivo, we used the Drosophila visual system. In this report, we describe a novel Drosophila mutant, alicorn (alc), encoding the single ␤ regulatory subunit of AMPK. Loss of alc using the eyFlp system causes severe early-onset progressive nonapoptotic neurodegeneration in the retina, the optic lobe, and the antennae, as well as behavioral and neurophysiological defects. Retinal degeneration occurs immediately after normal neuronal differentiation, can be enhanced by exposure to light, and can be prevented by blocking photoreceptor excitation. Furthermore, AMPK is required for proper viability of differentiated photoreceptors by mechanisms unrelated to polarity events that AMPK controls in epithelial tissues. In conclusion, AMPK does not affect photoreceptor development but is crucial to maintaining integrity of mature neurons under conditions of increased activity and provides protection from excitotoxicity.

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Mitochondrial enzyme activities as biochemical markers of aging

Cited by 77 publications

References 55 publications

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

Changes in mitochondrial energy utilization in young and old worker honeybees (Apis mellifera)

A large-scale screening of the normalized mammalian mitochondrial gene expression profiles

Drosophila alicorn Is a Neuronal Maintenance Factor Protecting against Activity-Induced Retinal Degeneration

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