Permeability of bilayer lipid membranes for superoxide (O2−) radicals

Gus'kova, Renata A.; Иванов, Ю.Н.; Kol'tover, Vitalij K.; Akhobadze, Victor V.; Rubin, A. B.

doi:10.1016/0005-2736(84)90409-7

Cited by 100 publications

(41 citation statements)

References 15 publications

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“…Given the extreme compartmentalization of the mitochondria and the limited ability of superoxide to diffuse through membranes (68,69), this raises the question of how the superoxide produced in the matrix contributes to the eNOS dysfunction and fibronectin accumulation that occur outside of the mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Nox4 NADPH Oxidase Mediates Peroxynitrite-dependent Uncoupling of Endothelial Nitric-oxide Synthase and Fibronectin Expression in Response to Angiotensin II

Lee¹,

Wauquier²,

Eid³

et al. 2013

Journal of Biological Chemistry

115

105

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Background: Oxidative stress is critical for the fibrotic response of mesangial cells (MCs) to angiotensin II. Results: Nox4-and mitochondrial reactive oxygen species (ROS)-dependent endothelial nitric-oxide synthase (eNOS) uncoupling led to fibronectin accumulation in MCs stimulated by angiotensin II. Conclusion: The Nox4/mitochondrial ROS/eNOS pathway mediates angiotensin II-induced MC injury. Significance: Targeting Nox4 and mitochondrial ROS is a promising therapeutic approach.

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Section: Discussionmentioning

confidence: 99%

Nox4 NADPH Oxidase Mediates Peroxynitrite-dependent Uncoupling of Endothelial Nitric-oxide Synthase and Fibronectin Expression in Response to Angiotensin II

Lee¹,

Wauquier²,

Eid³

et al. 2013

Journal of Biological Chemistry

115

105

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“…In the vesicles, the formation of superoxide is expect to be slow, and its migration from the cytosol to these vesicles is not probable to be significant because superoxide does not cross biomembranes, and so all superoxide that could cross the membrane would be in the form of the hydroperoxyl (Gus'kova et al, 1984), its protonated form. On the other hand, there is evidence of physical association between storage vesicles and mitochondria through tubular channels (Carmichael and Smith, 1978), and for the mitochondrial origin of the storage vesicles (Issidorides et al, 1996).…”

Section: Biological Relevance Of No and Dopamine Chemical Interactionsmentioning

confidence: 99%

Redox interactions of nitric oxide with dopamine and its derivatives

et al. 2005

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Nitric oxide ( • NO) is a ubiquitous diffusible messenger in the central nervous system. • NO and derived nitrogen species may interact with catecholamines, thus, modifying not only its regulatory actions but also producing oxidants and free radicals that are likely to trigger toxic pathways in the nervous system. Oxidative pathways and chain oxidation reactions triggered by catecholamines may be broken by ascorbate and glutathione, of which there is ample supply in the brain. At the subcellular level, mitochondria and cytosolic dopamine storage vesicles are likely to provide site-specific settings for • NO and catecholamines interactions. Thus, a complex picture emerges in which the steady-state levels of the individual reactants, the rate constants of the reactions involved, the oxygen tension, and the compartmentalization of reactions determine the biological significance of the redox interactions between • NO and dopamine metabolism in the brain. The physiological relevance of • NO-driven chemical modifications of dopamine and its derivatives and the ensuing free radical production are discussed in connection with the neurodegeneration inherent in Parkinson's disease.

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“…Mitochondrial superoxide is not likely to cross mitochondrial membranes (30) and yet it can influence extracellular pH by modulating organic acid production. In support of this effect of mitochondrial superoxide, we observed that the acid burst under long-term glycerol conditions is accelerated by sod2⌬ mutations lacking mitochondrial matrix Mn-SOD, but not by sod1⌬ mutations affecting the largely cytosolic Cu,Zn-SOD1.…”

Section: Discussionmentioning

confidence: 99%

“…In the bakers' yeast S. cerevisiae, cells lacking Sod2p are viable but are highly sensitive to hyperoxia and redox cycling agents (27)(28)(29), defects ascribed to increased superoxide damage to mitochondrial components. However, the means by which loss of yeast mitochondrial matrix Sod2p can control extracellular pH as described earlier (19) is not clear, particularly because the superoxide substrate for Sod2p should not cross the mitochondrial membranes (30).…”

mentioning

confidence: 99%

Superoxide Triggers an Acid Burst in Saccharomyces cerevisiae to Condition the Environment of Glucose-starved Cells

Baron¹,

Laws

Chen

et al. 2013

Journal of Biological Chemistry

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Background: During prolonged periods without glucose yeast cells acidify the extracellular environment. Results: This acid burst is derived from a mitochondrial aldehyde dehydrogenase and a cascade involving superoxide damage to the TCA cycle. Conclusion:The acid burst can condition the medium to improve cell growth. Significance: Damage from mitochondrial superoxide can be advantageous to cells during carbon starvation stress.

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Permeability of bilayer lipid membranes for superoxide (O2−) radicals

Cited by 100 publications

References 15 publications

Nox4 NADPH Oxidase Mediates Peroxynitrite-dependent Uncoupling of Endothelial Nitric-oxide Synthase and Fibronectin Expression in Response to Angiotensin II

Nox4 NADPH Oxidase Mediates Peroxynitrite-dependent Uncoupling of Endothelial Nitric-oxide Synthase and Fibronectin Expression in Response to Angiotensin II

Redox interactions of nitric oxide with dopamine and its derivatives

Superoxide Triggers an Acid Burst in Saccharomyces cerevisiae to Condition the Environment of Glucose-starved Cells

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