Fe2+ Induces a Transient Ca2+ Release from Rat Liver Mitochondria

Gogvadze, Vladimir; Walter, Patrick; Ames, Bruce N.

doi:10.1006/abbi.2001.2721

Cited by 10 publications

(5 citation statements)

References 28 publications

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“…Schipper and colleagues used histochemical analyses to visualize the age-associated sequestration of mitochondrial iron in human subcortical brain and in rat substantia nigra (Schipper & Cissé, 1995; Schipper et al ., 1998). Several other studies have suggested that mitochondrial damage via excessive cellular iron overload may be an intrinsic factor in mitochondrial permeability transition and the functional decline associated with aging (Gogvadze et al ., 2002, 2003; Walter et al ., 2002; Llorens et al ., 2007). However, no studies have investigated the accumulation of non-heme iron in mitochondria with age and the effects on oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

“…Past studies have indicated that advanced age renders mPTP more susceptible to oxidative stress and reduces the mitochondrial Ca 2+ -handling capacity (Kristal & Yu, 1998; Di Lisa & Bernardi, 2005). Similarly, iron-mediated oxidative stress has been shown to increase the susceptibility of mPTP against Ca 2+ stimuli (Gogvadze et al ., 2002, 2003). Therefore, it is possible that age-related accumulation of non-heme iron in mitochondria modulates mitochondrial oxidative stress and enhances permeability transition, which can potentially lead to cell death and tissue degeneration.…”

Section: Introductionmentioning

confidence: 99%

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Mitochondrial iron accumulation with age and functional consequences

et al. 2008

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Summary During the aging process, an accumulation of non-heme iron disrupts cellular homeostasis and contributes to the mitochondrial dysfunction typical of various neuromuscular degenerative diseases. Few studies have investigated the effects of iron accumulation on mitochondrial integrity and function in skeletal muscle and liver tissue. Thus, we isolated liver mitochondria (LM), as well as quadriceps-derived subsarcolemmal mitochondria (SSM) and interfibrillar mitochondria (IFM), from male Fischer 344× Brown Norway rats at 8, 18, 29 and 37 months of age. Non-heme iron content in SSM, IFM and LM was significantly higher with age, reaching a maximum at 37 months of age. The mitochondrial permeability transition pore (mPTP) was more susceptible to the opening in aged mitochondria containing high levels of iron (i.e. SSM and LM) compared to IFM. Furthermore, mitochondrial RNA oxidation increased significantly with age in SSM and LM, but not in IFM. Levels of mitochondrial RNA oxidation in SSM and LM correlated positively with levels of mitochondrial iron, whereas a significant negative correlation was observed between the maximum Ca2+ amounts needed to induce mPTP opening and iron contents in SSM, IFM and LM. Overall, our data suggest that age-dependent accumulation of mitochondrial iron may increase mitochondrial dysfunction and oxidative damage, thereby enhancing the susceptibility to apoptosis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Mitochondrial iron accumulation with age and functional consequences

et al. 2008

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“…In fact, excessive iron loading is known to perturb mitochondrial calcium homeostasis and to induce the release of calcium from this storage site (53). More recently, micromolar concentrations of ferrous iron were shown to cause a transient release of calcium from liver mitochondria without either damaging the organelle or decreasing its membrane potential, suggesting the physiological implication of iron-mediated calcium mobilization (54). Moreover, ONOO Ϫ at a low, physiologically relevant concentration (20 M), induced rapid intracellular mobilization of calcium in thymocytes (55).…”

Section: Lps and Peroxynitrite Increase Tyrosine Nitration Of I B␣-mentioning

confidence: 99%

Signaling Role of Intracellular Iron in NF-κB Activation

Xiong

She

Takeuchi

et al. 2003

Journal of Biological Chemistry

159

122

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“…A Ca 2+ -sensitive electrode was also used to determine [Ca 2+ ] m for broken mitochondria, as described [23]. In both assays calibration was obtained using known concentrations of Ca 2+ .…”

Section: Determination Of Intramitochondrial Calcium Concentrationmentioning

confidence: 99%

Hypoxia/Reoxygenation of isolated rat heart mitochondria causes cytochrome c release and oxidative stress; evidence for involvement of mitochondrial nitric oxide synthase

Zenebe

Nazarewicz

Parihar

et al. 2007

Journal of Molecular and Cellular Cardiology

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The objective of the present study was to delineate the molecular mechanisms for mitochondrial contribution to oxidative stress induced by hypoxia and reoxygenation in the heart. The present study introduces a novel model allowing real-time studying mitochondria under hypoxia and reoxygenation, and describes the significance of intramitochondrial calcium homeostasis and mitochondrial nitric oxide synthase (mtNOS) for oxidative stress. The present study shows that incubating isolated rat heart mitochondria under hypoxia followed by reoxygenation, but not hypoxia per se, causes cytochrome c release from the mitochondria, oxidative modification of mitochondrial lipids and proteins, and inactivation of mitochondrial enzymes susceptible to inactivation by peroxynitrite. Those alterations were prevented when mtNOS was inhibited or mitochondria were supplemented with antioxidant peroxynitrite scavengers. The present study shows mitochondria independent of other cellular components respond to hypoxia/reoxygenation by elevating intramitochondrial ionized calcium and stimulating mtNOS. The present study proposes a crucial role for heart mitochondrial calcium homeostasis and mtNOS in oxidative stress induced by hypoxia/ reoxygenation.

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Fe2+ Induces a Transient Ca2+ Release from Rat Liver Mitochondria

Cited by 10 publications

References 28 publications

Mitochondrial iron accumulation with age and functional consequences

Mitochondrial iron accumulation with age and functional consequences

Signaling Role of Intracellular Iron in NF-κB Activation

Hypoxia/Reoxygenation of isolated rat heart mitochondria causes cytochrome c release and oxidative stress; evidence for involvement of mitochondrial nitric oxide synthase

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