Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's disease

Bosetti, Francesca; Brizzi, Francesca; Barogi, Silvia; Mancuso, Michelangelo; Siciliano, Gabriele; Tendi, Elisabetta A.; Murri, Luigi; Rapoport, Stanley I.; Solaini, Giancarlo

doi:10.1016/s0197-4580(01)00314-1

Cited by 329 publications

(208 citation statements)

References 58 publications

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“…Although the etiology of Alzheimer's disease (AD) is multifactoral (Prasad et al, 2002), a consistent finding is hypometabolism of glucose in those brain regions affected by the disease (Bosetti et al, 2002) that can be detected very early in the disease, even before cognitive symptoms are reported (Hirai et al, 2001;Blass, 2003). Although hypometabolism may simply reflect neuronal loss in the effected regions, mitochondrial dysfunction can be more directly implicated in AD.…”

Section: Mitochondrial Function In Neurodegenerative Diseasesmentioning

confidence: 99%

Estrogen actions on mitochondria—Physiological and pathological implications

Simpkins

Yang

Sarkar

et al. 2008

Molecular and Cellular Endocrinology

132

105

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Estrogens are potent neuroprotective hormones and mitochondria are the site of cellular life-death decisions. As such, it is not surprising that we and other have shown that estrogens have remarkable effects on mitochondrial function. Herein we provide evidence for a primary effect of estrogens on mitochondrial function, achieved in part by the import of estrogen receptor β (ERβ) into the mitochondria where it mediates a number of estrogen actions on this vital organelle. ERβ is imported into the mitochondria, through tethering to cytosolic chaperone protein and/or through direct interaction with mitochondrial import proteins. In the mitochondria, ERβ can affect transcription of critical mitochondrial genes through the interaction with estrogen response elements (ERE) or through protein-protein interactions with mitochondrially imported transcription factors. The potent effects of estrogens on mitochondrial function, particularly during mitochondrial stress, argues for a role of estrogens in the treatment of mitochondrial defects in chronic neurodegenerative diseases like Alzheimer's disease (AD) and Parkinson's disease (PD) and more acute conditions of mitochondrial compromise, like cerebral ischemia and traumatic brain injury.

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Section: Mitochondrial Function In Neurodegenerative Diseasesmentioning

confidence: 99%

Estrogen actions on mitochondria—Physiological and pathological implications

Simpkins

Yang

Sarkar

et al. 2008

Molecular and Cellular Endocrinology

132

105

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“…Oxidative stress has been implicated in many neurodegenerative disorders, including Alzheimer's disease (AD) [1][2][3][4], AD is characterized clinically by progressive dementia and pathologically by extracellular amyloid protein deposits, intracellular neurofibrilary tangles (NFTs) (composed mostly of hyperphosphorylated tau protein), loss of synapses, mitochondrial dysfunction and programmed cell death (PCD) [5,6]. The reduced energy metabolism in AD may be due to oxidative dysfunction of some of the key metabolic or mitochondrial enzymes [7][8][9][10][11][12], which may lead to increased reactive oxygen species (ROS) production.…”

Section: Introductionmentioning

confidence: 99%

“…Amyloid deposition, oxidative stress, mitochondria DNA deletion and mitochondrial structural and functional abnormalities are prominent in AD [5,13,14]. Many pro-apoptotic signals and anti-apoptotic defenses converge in the mitochondria [15].…”

Section: Introductionmentioning

confidence: 99%

“…It is now well known that ROS such as superoxide anion (O 2 -), hydroxyl radical (OH), hydrogen peroxide (H 2 O 2 ), and peroxynitrite (ONOO -) contribute to neurodegeneration [21,[24][25][26][27][28]. Mitochondrial membrane potential depolarization induces cytochrome-c release into the cytoplasm and elevates the activity of caspase-3, suggesting a role for mtDNA-derived mitochondrial dysfunction in AD degeneration [5].…”

Section: Introductionmentioning

confidence: 99%

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In vivo administration of D609 leads to protection of subsequently isolated gerbil brain mitochondria subjected to in vitro oxidative stress induced by amyloid beta-peptide and other oxidative stressors: Relevance to Alzheimer’s disease and other oxidative stress-related neurodegenerative disorders

Ansari

Joshi

Huang

et al. 2006

Free Radical Biology and Medicine

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Tricyclodecan-9-yl-xanthogenate (D609) has in vivo and in vitro antioxidant properties. D609 mimics glutathione (GSH), has a free thiol group, which upon oxidation forms a disulfide. The resulting dixanthate is a substrate for glutathione reductase, regenerating D609. Recent studies have also shown that D609 protects brain in vivo and neuronal cultures in vitro against the potential Alzheimer's disease (AD) causative factor, Aβ (1-42)-induced oxidative stress and cytotoxicity. Mitochondria are important organelles with both pro-and anti-apoptotic factor proteins. The present study was undertaken to test the hypothesis that i.p. injection of D609 would provide neuroprotection against free radical-induced, mitochondria-mediated apoptosis in vitro. Brain mitochondria were isolated from gerbils 1 h post injection intraperitonially (i.p.) with D609 and subsequently treated in vitro with the oxidants Fe 2+ /H 2 O 2 (hydroxyl free radicals), 2,2-azobis-(2-amidinopropane) dihydrochloride (AAPH, alkoxyl and peroxyl free radicals) and AD-relevant amyloid β-peptide 1-42 [Aβ (1-42)]. Brain mitochondria isolated from the gerbils previously injected i.p. with D609 and subjected to these oxidative stress inducers, in vitro, showed significant reduction in levels of protein carbonyls, protein-bound hydroxynonenal (HNE) [a lipid peroxidation product], 3-nitrotyrosine (3-NT), and cytochrome-c release compared to oxidant-treated brain mitochondria isolated from salineinjected gerbils. D609 treatment significantly maintains the GSH/GSSG ratio in oxidant-treated mitochondria. Increased activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx) and glutathione reductase (GR) in brain isolated from D609-injected gerbils is consistent with the notion that D609 acts like GSH. These anti-apoptotic findings are discussed with reference to the potential use of this brain-accessible glutathione mimetic in the treatment of oxidative stress-related neurodegenerative disorders, including AD.

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“…Even though they do not participate on the energetic turnover in the whole organism as much as muscle fibers or neurons, the changes in activities of respiratory chain complexes in isolated platelets have already been described in the patients with classical mitochondrial diseases e.g. with intermittent ataxia and lactate acidosis 12 and Leber's hereditary optic neuropathy 13 or in small groups of patients with Huntington disease, 14 Parkinson disease, [15][16][17] and Alzheimer disease, 18 where the disturbances in activities of respiratory chain complexes were probably a secondary effect.…”

Section: Introductionmentioning

confidence: 99%

Activities of respiratory chain complexes in isolated platelets in females with anorexia nervosa

Böhm

Papežová

Hansı́ková

et al. 2007

Intl J Eating Disorders

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Objective: A broad spectrum of endocrine and biochemical disturbances was observed in patients with anorexia nervosa. In addition, metabolic changes may concern the efficiency of mitochondrial energy generating system. In our study we analyzed the activities of respiratory chain complexes in females with anorexia nervosa.Method: The activities of respiratory chain complexes I, II, IV, I 1 III, and citrate synthase serving as the control enzyme were measured spectrophotometrically in isolated platelets in 36 females with anorexia nervosa (BMI 15 6 1.7) at the age 18-35 years and in 37 age related female controls (BMI 21 6 2.2).Results: In females with anorexia nervosa, the activities of respiratory chain complexes I and II in isolated platelets were significantly higher in comparison with controls. No differences were found in the activities of complexes IV and I 1 III and citrate synthase. Conclusion:Our results suggest higher efficiency of some respiratory chain complexes in platelets in females with anorexia nervosa. V V C 2007 by Wiley Periodicals, Inc.

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Cytochrome c oxidase and mitochondrial F1F0-ATPase (ATP synthase) activities in platelets and brain from patients with Alzheimer's disease

Cited by 329 publications

References 58 publications

Estrogen actions on mitochondria—Physiological and pathological implications

Estrogen actions on mitochondria—Physiological and pathological implications

Activities of respiratory chain complexes in isolated platelets in females with anorexia nervosa

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