Calcium-induced generation of reactive oxygen species in brain mitochondria is mediated by permeability transition

Hansson, Magnus; Månsson, Roland; Morota, Saori; Uchino, Haruto; Kallur, Therése; Sumi, Tetsuo; Ishii, Nagao; Shimazu, Motohide; Keep, Marcus F.; Jegorov, Alexandr; Elmér, Eskil

doi:10.1016/j.freeradbiomed.2008.04.021

Cited by 106 publications

(71 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). Substantial evidence in the literature has indicated that Ca 2+ can increase mitochondrial oxidative stress (15). In line with this, Ca 2+ increased the rate of DCFH oxidation compared to the control.…”

Section: Resultssupporting

confidence: 62%

In vitro antioxidant activity of stem bark of Trichilia catigua Adr. Juss

Kamdem¹,

Stefanello²,

Boligon³

et al. 2012

Acta Pharmaceutica

View full text Add to dashboard Cite

Antioxidant activity of the ethanolic extract and fractions from the stem bark of T. catigua was investigated. IC 50 (for DPPH scavenging) by T. catigua varied from 9.17 ± 0.63 to 76.42 ± 5.87 mg mL -1 and total phenolic content varied from 345.63 ± 41.08 to 601.27 ± 42.59 mg GAE g -1 of dry extract. Fe 2+ -induced lipid peroxidation was significantly reduced by the ethanolic extract and fractions. Mitochondrial Ca 2+ -induced dichlorofluorescein oxidation was significantly reduced by the ethanolic extract in a concentration-dependent manner. Ethanolic extract reduced mitochondrial Dy m only at high concentrations (40-100 mg mL -1 ), which indicates that its toxicity does not overlap with its antioxidant effects. Results suggest involvement of antioxidant activities of T. catigua in its pharmacological properties.

show abstract

Section: Resultssupporting

confidence: 62%

In vitro antioxidant activity of stem bark of Trichilia catigua Adr. Juss

Kamdem¹,

Stefanello²,

Boligon³

et al. 2012

Acta Pharmaceutica

View full text Add to dashboard Cite

show abstract

“…Calcium-overload, excitotoxicity, ER stress and oxidative injury, and caspase-mediated apoptosis have been implicated as major injury mechanisms [35,36] .…”

Section: Mechanisms Of Autophagy Activation In Ischemic And/or Hypoximentioning

confidence: 99%

Death and survival of neuronal and astrocytic cells in ischemic brain injury: a role of autophagy

Zhang

2011

Acta Pharmacol Sin

View full text Add to dashboard Cite

Autophagy is a highly regulated cellular mechanism that leads to degradation of long-lived proteins and dysfunctional organelles. The process has been implicated in a variety of physiological and pathological conditions relevant to neurological diseases. Recent studies show the existence of autophagy in cerebral ischemia, but no consensus has yet been reached regarding the functions of autophagy in this condition. This article highlights the activation of autophagy during cerebral ischemia and/or reperfusion, especially in neurons and astrocytes, as well as the role of autophagy in neuronal or astrocytic cell death and survival. We propose that physiological levels of autophagy, presumably caused by mild to modest hypoxia or ischemia, appear to be protective. However, high levels of autophagy caused by severe hypoxia or ischemia and/or reperfusion may cause self-digestion and eventual neuronal and astrocytic cell death. We also discuss that oxidative and endoplasmic reticulum (ER) stresses in cerebral hypoxia or ischemia and/or reperfusion are potent stimuli of autophagy in neurons and astrocytes. In addition, we review the evidence suggesting a considerable overlap between autophagy on one hand, and apoptosis, necrosis and necroptosis on the other hand, in determining the outcomes and final morphology of damaged neurons and astrocytes.

show abstract

“…Cell culture studies show that excess glutamate receptor activation in neurons can cause increased intracellular Ca 2+ , mitochondrial ROS production, bioenergetic failure, and mitochondrial trafficking abnormalities [130]. Ca 2+ -induced generation of ROS in brain mitochondria is mediated by mitochondrial permeability transition [131]. Motor neurons are particularly affected by inhibition of mitochondrial metabolism, which can cause elevated cytosolic Ca 2+ levels and increased excitability [132].…”

Section: Fig 3 Motor Neurons In Spinal Cord Degenerate In People Wimentioning

confidence: 99%

Mitochondrial Pathobiology in Parkinson's Disease and Amyotrophic Lateral Sclerosis

Martin

2010

JAD

View full text Add to dashboard Cite

Abstract. Parkinson's disease (PD) and amyotrophic lateral sclerosis (ALS) are the second and third most common human adult-onset neurodegenerative diseases, respectively, after Alzheimer's disease. They are characterized by prominent age-related neurodegeneration in selectively vulnerable neural systems. Some forms of PD and ALS are inherited, and genes causing these diseases have been identified. Morphological, biochemical, and genetic, as well as cell and animal model, studies reveal that mitochondria could have a role in this neurodegeneration. The functions and properties of mitochondria might render subsets of selectively vulnerable neurons intrinsically susceptible to cellular aging and stress and overlying genetic variations. In PD, mutations in putative mitochondrial proteins have been identified and mitochondrial DNA mutations have been found in neurons in the substantia nigra. In ALS, changes occur in mitochondrial respiratory chain enzymes and mitochondrial cell death proteins. Transgenic mouse models of human neurodegenerative disease are beginning to reveal possible principles governing the biology of selective neuronal vulnerability that implicate mitochondria and the mitochondrial permeability transition pore. This review will present how mitochondrial pathobiology might contribute to neurodegeneration in PD and ALS and could serve as a target for drug therapy.

show abstract

Calcium-induced generation of reactive oxygen species in brain mitochondria is mediated by permeability transition

Cited by 106 publications

References 53 publications

In vitro antioxidant activity of stem bark of Trichilia catigua Adr. Juss

In vitro antioxidant activity of stem bark of Trichilia catigua Adr. Juss

Death and survival of neuronal and astrocytic cells in ischemic brain injury: a role of autophagy

Mitochondrial Pathobiology in Parkinson's Disease and Amyotrophic Lateral Sclerosis

Contact Info

Product

Resources

About