Membrane changes associated with lysis of red blood cells by hypochlorous acid

Vissers, Margreet C.M.; Stern, Arnold; Kuypers, Frans A.; Berg, J. Van Den; Winterbourn, Christine C.

doi:10.1016/0891-5849(94)90185-6

Cited by 83 publications

(64 citation statements)

References 29 publications

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“…These particular oxidants were chosen because of the qualitative differences in oxidative challenge that they present to the red cell. XO/HO mixtures generate SOA and hydrogen peroxide extracellularly (Baskurt et al , 1998; Rogers et al , 2009), whilst PMS generates SOA intracellularly (Nishikimi et al , 1972; Maridonneau et al , 1983); NO 2 oxidises Hb to metHb (Muzyamba et al , 2000); t BHP increases generation of peroxyl and alkoxyl free radicals (Davies, 1989); whilst HOCl produced by myeloperoxidase released from neutorphils may also oxidise membrane thiols (Vissers et al , 1994; Gorudko et al , 2016). Red cell PS exposure is most reliably stimulated by elevation of intracellular Ca 2+ (Bevers & Williamson, 2010) whilst a number of oxidants have previously been shown to increase red cell cation permeability (Gibson & Muzyamba, 2003a,2003b).…”

Section: Discussionmentioning

confidence: 99%

“…This is particularly significant in diseases such as SCA in which vascular oxidative stress is increased (Rice‐Evans et al , 1986) with accumulations of highly reactive oxygen species (ROS) including the superoxide anion, hydrogen peroxide and the hydroxyl radical (Sies, 1997; Chirico & Pialoux, 2012; Voskou et al , 2015). Myeloperoxidase released from activated neutrophils may also add to oxidant challenge in SCA, through production of hypochlorous acid (HOCl) from hydrogen peroxide (Vissers et al , 1994; Mutze et al , 2003; Zhang et al , 2013). Thiol oxidation has also been associated with both inhibition of the flippase and stimulation of the scramblase (Morrot et al , 1989; Connor & Schroit, 1990; Devaux & Zachowski, 1994; Martin & Jesty, 1995; de Jong & Kuypers, 2006).…”

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confidence: 99%

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Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

et al. 2018

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SummaryPhosphatidylserine (PS) exposure increases as red cells age, and is an important signal for the removal of senescent cells from the circulation. PS exposure is elevated in red cells from sickle cell anaemia (SCA) patients and is thought to enhance haemolysis and vaso‐occlusion. Although precise conditions leading to its externalisation are unclear, high intracellular Ca2+ has been implicated. Red cells from SCA patients are also exposed to an increased oxidative challenge, and we postulated that this stimulates PS exposure, through increased Ca2+ levels. We tested four different ways of generating oxidative stress: hypoxanthine and xanthine oxidase, phenazine methosulphate, nitrite and tert‐butyl hydroperoxide, together with thiol modification with N‐ethylmaleimide (NEM), dithiothreitol and hypochlorous acid (HOCl), in red cells permeabilised to Ca2+ using bromo‐A23187. Unexpectedly, our findings showed that the four oxidants significantly reduced Ca2+‐induced PS exposure (by 40–60%) with no appreciable effect on Ca2+ affinity. By contrast, NEM markedly increased PS exposure (by about 400%) and slightly but significantly increased the affinity for Ca2+. Dithiothreitol modestly reduced PS exposure (by 25%) and HOCl had no effect. These findings emphasise the importance of thiol modification for PS exposure in sickle cells but suggest that increased oxidant stress alone is not important.

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Section: Discussionmentioning

confidence: 99%

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confidence: 99%

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

et al. 2018

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“…Lysis was measured either by continuous monitoring of A (!! or by measuring the haemoglobin concentration of the supernatant after centrifugation [27]. Oxidant solutions were added to cell suspensions at room temperature ; any subsequent incubations were at 37 mC.…”

Section: Red Cell Lysis With Hocl and Hobrmentioning

confidence: 99%

“…Oxidant solutions were added to cell suspensions at room temperature ; any subsequent incubations were at 37 mC. We have previously shown that the rate of lysis is dependent on the dose of HOCl per cell rather than on the concentration of oxidant [27], and the results are therefore expressed as nmol of oxidant per 10( cells. In most experiments we used 2.5 % (w\v) cell suspensions with 100-2500 µM oxidant.…”

Section: Red Cell Lysis With Hocl and Hobrmentioning

confidence: 99%

“…However, the mechanism by which HOCl causes lysis is not known. We have shown previously that haemolysis occurs by a colloid osmotic mechanism that involves disruption of the membrane to cause K + leakage and swelling [14,27]. Although reduced glutathione (GSH) and membrane thiols were easily oxidized, this was not associated with lysis and the critical target remains unidentified.…”

Section: Introductionmentioning

confidence: 99%

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Comparison of human red cell lysis by hypochlorous and hypobromous acids: insights into the mechanism of lysis

Vissers

Carr

Chapman

1998

Biochemical Journal

103

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Human red blood cells are lysed by the neutrophil-derived oxidant hypochlorous acid (HOCl), although the mechanism of lysis is unknown. Hypobromous acid (HOBr), a similarly reactive oxidant, lysed red cells approx. 10-fold faster than HOCl. Therefore we compared the effects of these oxidants on thiols, membrane lipids and proteins to determine which reactions are associated with lysis. There was no difference in the loss of reduced glutathione or membrane thiols with either oxidant, but HOBr reacted more readily with membrane lipids and proteins. Bromohydrin derivatives of phospholipids and cholesterol were seen at approx. one-tenth the level of oxidant than chlorohydrins were. However, these products were detected only with high concentrations of HOCl or HOBr, which caused instant haemolysis. Membrane protein modification occurred at much lower doses of oxidant and was more closely correlated with lysis. SDS/PAGE analysis showed that band 3, the anion transport protein, was lost at the lowest dose of HOBr and at the higher concentrations of HOCl. Labelling the red cells with eosin 5-maleimide, a fluorescent label for band 3, suggested possible clustering of this protein in oxidant-exposed cells. There was also irreversible cross-linking of all the major membrane proteins; this reaction occurred more readily with HOBr. The results indicate that membrane protein modification is the reaction responsible for HOCl-mediated lysis. These effects, and particularly cross-link formation, might result in clustering of band 3 and other membrane and cytoskeletal proteins to form haemolytic pores.

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In vitro protective effect of Rhodiola rosea extract against hypochlorous acid‐induced oxidative damage in human erythrocytes

et al. 2004

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Rhodiola rosea L. (Crassulaceae) is a plant living at high altitudes in Europe and Asia. Its roots have long been used in the traditional medical system of these geographical areas to increase the organism resistance to physical stress; today, it has become an important component of many dietary supplements. In this study we investigate the antioxidant capacity of the R. rosea aqueous extract evaluating its ability to counteract some of the main damages induced by hypochlorous acid (HOCl), a powerful oxidant generated by activated phagocytes, to human erythrocytes. Ascorbic acid was used as a reference substance because of its physiological HOCl-scavenging ability. Our study demonstrates that R. rosea is able to significantly protect, in a dose-dependent manner, human RBC from glutathione (GSH) depletion, glyceraldehyde-3-phosphate dehydrogenase (GAPDH) inactivation and hemolysis induced by the oxidant. Furthermore, we demonstrate that R. rosea aqueous extract acts from the inside of the erythrocyte suggesting a probable involving of cell components. The protection on GSH afforded by the R. rosea extract with respect to ascorbic acid, occurred also if added 2 or 5 min. later than the oxidant, suggesting a more rapid or powerful effect.

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Membrane changes associated with lysis of red blood cells by hypochlorous acid

Cited by 83 publications

References 29 publications

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia

Comparison of human red cell lysis by hypochlorous and hypobromous acids: insights into the mechanism of lysis

In vitro protective effect of Rhodiola rosea extract against hypochlorous acid‐induced oxidative damage in human erythrocytes

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