Oxidative stress of human erythrocytes by iodate and periodate Reversible formation of aqueous membrane pores due to SH-group oxidation

Heller, Klaus B.; Poser, Barbara; Haest, C.W.M.; Deüticke, B.

doi:10.1016/0005-2736(84)90502-9

Cited by 34 publications

(5 citation statements)

References 28 publications

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“…We know that paraquat exposure results in an elevated state of oxidative stress and compromised mitochondrial energy production via redox cycling targeting the mitochondrial electron transport chain (Fig. 6, steps 4 & 5; (Heller et al, 1984; Day et al, 1999; Macianskiene et al, 2001; Lim et al, 2002; Yumino et al, 2002; McCormack et al, 2005; Cocheme and Murphy, 2008; Pamplona, 2008)). Lastly, α-synuclein is localized to the membrane where it also promotes membrane dysfunction cumulatively leading to enhance membrane conductance (Fig.…”

Section: Discussionmentioning

confidence: 99%

Dopamine and Paraquat Enhance α-Synuclein-Induced Alterations in Membrane Conductance

Feng

Maguire‐Zeiss

2011

Neurotox Res

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We have previously demonstrated that α-synuclein overexpression increases the membrane conductance of dopaminergic-like cells. Although α-synuclein is thought to play a central role in the pathogenesis of several neurodegenerative diseases including Parkinson’s disease, multiple system atrophy and diffuse Lewy body disease the mechanism of action is not completely understood. In this study we sought to determine whether multiple factors act together with α-synuclein to engender cell vulnerability through an augmentation of membrane conductance. Here we employed a cell model that mimics dopaminergic neurons coupled with α-synuclein overexpression and oxidative stressors. We demonstrate an enhancement of α-synuclein-induced toxicity in the presence of combined treatment with dopamine and paraquat, two molecules known to incite oxidative stress. In addition we show that combined dopamine and paraquat treatment increases the expression of heme oxygenase-1, an antioxidant response protein. Finally, we demonstrate for the first time that combined treatment of dopaminergic cells with paraquat and dopamine enhances α-synuclein-induced leak channel properties resulting in increased membrane conductance. Importantly, these increases are most robust when both paraquat and dopamine are present suggesting the need for multiple oxidative insults to augment α-synuclein-induced disruption of membrane integrity.

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Section: Discussionmentioning

confidence: 99%

Dopamine and Paraquat Enhance α-Synuclein-Induced Alterations in Membrane Conductance

Feng

Maguire‐Zeiss

2011

Neurotox Res

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“…In this respect low temperature, high hydrostatic pressure and SH-reactive reagents could be of some interest. There is a significant literature on cation fluxes induced by SH-reactive reagents including PCMBS, diamide and periodate (Knauf & Rothstein, 1971;Deuticke, Poser, Liitkemeier & Haest, 1983;Heller, Poser, Haest & Deuticke, 1984;Haas & Schmidt, 1985). However, a substantial portion of the PCMBS-induced cation fluxes shows a specific anion requirement for Cl-or Br- (Haas & Schmidt, 1985) which is different from the low ionic strength-stimulated cation fluxes.…”

Section: Temperature Dependence and Influence Of Monovalent Cationsmentioning

confidence: 99%

Effects of low ionic strength media on passive human red cell monovalent cation transport.

Bernhardt¹,

Hall²,

Ellory³

1991

The Journal of Physiology

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SUMMARY1. The effect of low ionic strength media on the residual, i.e. (ouabain + bumetanide+ Ca2+)-insensitive, K+ influx was characterized in human red blood cells.2. This K+ flux was enhanced significantly in isotonic solutions of low ionic strength using sucrose to maintain constant osmolarity. This effect was found for fresh red blood cells as well as for stored (bank) red blood cells. However, the absolute magnitude of K+ influx in solutions of low ionic strength was halved for stored red blood cells.3. Anion replacement of Cl-by CH3SO4-did not affect residual K+ fluxes, showing that Cl-dependent transport pathways (e.g. the KCl co-transporter) are not involved in the low ionic strength effect.4. The enhanced K+ influx in low ionic strength media was reversible when the cells were resuspended in a solution of physiological ionic strength.5. K+ influx measured in light and dense fractions of erythrocytes (separated by centrifugation and corresponding to samples enriched with either 'young' or 'mature' red cells) showed that the low ionic strength effect does not change markedly with cell age.6. Low ionic strength media elevated residual, i.e. (ouabain + bumetanide + Ca2+)-insensitive, influx of both K+ and Na+ by about the same amount. In both cases the flux was linear with concentration in the range investigated (025-10 mM). No significant increase in the uptake of the cations Ca2+ and lysine in low ionic strength solutions could be found.7. In CH3S04--containing solutions of physiological ionic strength the residual K+ influx was almost independent of cell volume, whereas this flux in CH3S04--containing solutions of low ionic strength declined as cell volume was increased.8. K+ flux measurements in solutions of different external pH, where NaCl was replaced by sodium gluconate or sodium glucuronate, showed that the reduced ionic strength is of more importance for the enhanced residual K+ influx than the changed transmembrane potential or the changed intracellular pH. However, a small pH dependence could be found, the K+ flux passing through a minimum around pHi 7.3.9.

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“…Non-specific leaks usually contribute little to the total permeability of polar substances. However, leaks can be induced in artificial lipid membranes or red cells by brief electrical discharges (Schwister & Deuticke, 1985), covalent modification of SH groups by diamide and tetrathionate (Deuticke, Poser, Lutkemeier & Haest, 1983), oxidation by periodate/iodate (Heller, Poser, Haest & Deuticke, 1984) or <-butyl hydroperoxide (Deuticke, Heller & Haest, 1986), and exposure to amphipaths such as chlorpromazine (Lieber, Lange, Weinstein & Steck, 1984). The leaks are capable of discriminating amongst monovalent inorganic anions, between mono-and dicarboxylates of equal chain length, and between members of the same class with differing chain lengths.…”

Section: Aqueous Membrane Leaksmentioning

confidence: 99%

The Wellcome Trust Lecture: Mechanisms of molecular trafficking in malaria

Sherman

1988

Parasitology

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SUMMARYThe asexual stages ofPlasmodiumliving within the erythrocyte result in growth-related changes in the permeability properties of the red cell for substances such as glucose, amino acids, purine nucleosides, sodium, potassium, calcium, zinc, iron and several antimalarial drugs such as chloroquine, amodiaquine and mefloquine. In most cases such changes do not appear to be due to a modification in the affinity or specificity of red cell transporters; indeed, for most substances the membrane-associated transporters are either unaffected or are partially inactivated. In malaria-infected erythrocytes, where a striking increase in influx has been observed, it has been attributed to the insertion of parasite-encoded transporters into the red cell membrane or the formation of aqueous leaks and/or pores. Leak formation, in the vast majority of cases, does not appear to be dependent on the insertion of plasmodial proteins into the red cell membrane. However, since the data presently available are less than satisfactory for discriminating amongst the various possible transport mechanisms future studies will require painstaking efforts and carefully controlled conditions to discriminate amongst the various transport systems which are operational in the malaria-infected red cell and the parasite.

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Oxidative stress of human erythrocytes by iodate and periodate Reversible formation of aqueous membrane pores due to SH-group oxidation

Cited by 34 publications

References 28 publications

Dopamine and Paraquat Enhance α-Synuclein-Induced Alterations in Membrane Conductance

Dopamine and Paraquat Enhance α-Synuclein-Induced Alterations in Membrane Conductance

Effects of low ionic strength media on passive human red cell monovalent cation transport.

The Wellcome Trust Lecture: Mechanisms of molecular trafficking in malaria

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