Mitochondrial activities of rat heart during ageing

Castelluccio, Cinzia; Baracca, Alessandra; Fato, Romana; Pallotti, Francesco; Maranesi, Magda; Barzanti, V.; Gorini, A.; Villa, R. F.; Castelli, Giovanna Parenti; Marchetti, M.; Lenaz, Giorgio

doi:10.1016/0047-6374(94)91583-0

Cited by 36 publications

(23 citation statements)

References 40 publications

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“…In addition, a greater decline in activity with age was observed in wild-type mice versus Ames mice in all tissues examined. There are many reports confirming that complex I activities decline with aging and that this decline contributes to the reduction in mitochondrial respiration with aging (Castelluccio et al 1994;Ventura et al 2002;Cooper et al 1992;Sugiyama et al 1993). It has been proposed that complex I therefore, may become more rate controlling with age (Ventura et al 2002).…”

Section: Discussionmentioning

confidence: 99%

Expression of oxidative phosphorylation components in mitochondria of long-living Ames dwarf mice

Brown‐Borg

Johnson

Rakoczy

2011

AGE

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Reduced signaling of the growth hormone (GH)/insulin-like growth factor-1 (IGF-1) pathway is associated with extended life span in several species. Ames dwarf mice are GH-deficient and live >50% longer than wild-type littermates. Previously, we have shown that tissues from Ames mice exhibit elevated levels of antioxidative enzymes, less H 2 O 2 production, and lower oxidative damage suggesting that mitochondrial function may differ between genotypes. To explore the relationship between hormone deficiency and mitochondria in mice with extended longevity, we evaluated activity, protein, and gene expression of oxidative phosphorylation components in dwarf and wild-type mice at varying ages. Liver complex I+III activity was higher in dwarf mice compared to wildtype mice. The activity of I+III decreased between 3 and 20 months of age in both genotypes with greater declines in wild-type mice in liver and skeletal muscle. Complex IV activities in the kidney were elevated in 3-and 20-month-old dwarf mice relative to wild-type mice. In Ames mice, protein levels of the 39 kDa complex I subunit were elevated at 20 months of age when compared to wild-type mouse mitochondria for every tissue examined. Kidney and liver mitochondria from 20-month-old dwarf mice had elevated levels of both mitochondrially-encoded and nuclear-encoded complex IV proteins compared to wild-type mice (p<0.05). Higher liver ANT1 and PGC-1α mRNA levels were also observed in dwarf mice. Overall, we found that several components of the oxidative phosphorylation (OXPHOS) system were elevated in Ames mice. Mitochondrial to nuclear DNA ratios were not different between genotypes despite the marked increase in PGC-1α levels in dwarf mice. The increased OXPHOS activities, along with lower ROS production in dwarf mice, predict enhanced mitochondrial function and efficiency, two factors likely contributing to long-life in Ames mice.

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Section: Discussionmentioning

confidence: 99%

Expression of oxidative phosphorylation components in mitochondria of long-living Ames dwarf mice

Brown‐Borg

Johnson

Rakoczy

2011

AGE

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“…The vicious cycle theory proposes that progressive accumulations of ROS-induced somatic mutations in mtDNA may result in dysfunctions of respiratory chain, leading to increased production of ROS and subsequent accumulation of more mtDNA mutations as one of the reasons for increase in oxidative damage during aging (Linnane et al 1989;Wei 1992). Complex I is generally reported to be impaired with age in cardiac mitochondria (Castelluccio et al 1994). According to the mitochondrial theory of aging, the highest frequency of mutations would affect Complex I and secondarily Complex IV, for which respectively seven and three mitochondrial genes are present (Miquel et al 1980).…”

Section: Body Weight (G)mentioning

confidence: 99%

Ganoderma lucidum (Fr.) P. Karst enhances activities of heart mitochondrial enzymes and respiratory chain complexes in the aged rat

2009

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Aging is associated with increased oxidative damage at multiple cellular levels, decline in cellular energy production and enhanced free radical status. The effect of the medicinal mushroom, Ganoderma lucidum on the activities of tricarboxylic acid (Krebs) cycle enzymes and mitochondrial complexes I-IV of the electron transport chain in aged rats were investigated. The activity of Krebs cycle enzymes, isocitrate dehydrogenase, alpha-ketoglutarate dehydrogenase, succinate dehydrogenase, and malate dehydrogenase as well as mitochondrial complexes I, II, III, and IV were determined in heart of aged male Wistar rats orally administrated with 70% ethanolic extract (50 and 250 mg/kg) of G. lucidum. DL-alpha-lipoic acid (100 mg/kg) was taken as the positive control. Administration of the G. lucidum, once daily for 15 days, was significantly (P < 0.05) effective to enhance the Krebs cycle dehydrogenases, and mitochondrial electron transport chain complex IV activities in aged rats. The profound activity of the extract can be correlated to the significant antioxidant property of G. lucidum. The results of the study revealed that G. lucidum is effective to ameliorate the age associated decline of cellular energy status.

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“…The Complex I enzymatic activity was assayed at 258 after one cycle of freezing and thawing of the isolated mitochondria stored at 280 8C as described by Castelluccio et al [24].…”

Section: Enzymatic Determinationsmentioning

confidence: 99%

Impairment of mitochondrial oxidative phosphorylation in rat fatty liver exposed to preservation-reperfusion injury

Caraceni¹,

Bianchi²,

Domenicali³

et al. 2004

Journal of Hepatology

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Mitochondrial activities of rat heart during ageing

Cited by 36 publications

References 40 publications

Expression of oxidative phosphorylation components in mitochondria of long-living Ames dwarf mice

Expression of oxidative phosphorylation components in mitochondria of long-living Ames dwarf mice

Ganoderma lucidum (Fr.) P. Karst enhances activities of heart mitochondrial enzymes and respiratory chain complexes in the aged rat

Impairment of mitochondrial oxidative phosphorylation in rat fatty liver exposed to preservation-reperfusion injury

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