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Effect of exogenous hydrogen peroxide on human erythrocytes



Circulating erythrocytes are drastically susceptible to peroxidative reactions. To examine the extent of the damage induced by exogenous H2O2 we limited the catalase activity in order to study the extent of lysis, the lipid peroxidation and namely the behaviour of membrane micro-viscosity. Our data showed that the erythrocytes can efficiently scavenge exogenous H2O2 without significant damage of the cells and/or their membranes. These findings could confirm the important role of the erythrocytes as extracellular-antioxidant defense.
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Biblioteca richiedente: Facoltà di Medicina e Chirurgia- Università degli Studi dell'Aquila
Data richiesta: 03/07/2015 10:59:35
Biblioteca fornitrice: Biblioteca Interdipartimentale di Medicina - Biblioteca Biomedica
Data evasione: 07/07/2015 12:12:59
Titolo rivista/libro: Cellular and molecular biology
Titolo articolo/sezione: Effect of exogenous hydrogen peroxide on human erythrocytes
Autore/i: Tozzi-Ciancarelli MG, Di Massimo C, D'Orazio MC, Mascioli A, Di Giulio A, Tozzi E
ISSN: 0145-5680
Anno: 1990
Volume: 36
Fascicolo: 1
Pag. iniziale: 57
Pag. finale: 64
... Because blood H 2 O 2 is significantly elevated in sepsis, the bidirectionality of H 2 O 2 cell-membrane permeability implies a similar H 2 O 2 load within the intracellular compartment (van Asbeck et al. 1995). Due to its significant reductive capacity derived from reduced thiols in serum albumin and erythrocyte glutathione, whole blood normally functions as a physiological redox sink for H 2 O 2 diffusing from the intracellular compartment into the systemic circulation (Roche et al. 2008;Cha and Kim 1996;Tozzi-Ciancarelli et al. 1990). Consequently, systemically elevated H 2 O 2 indicates depletion of reductive capacity in whole blood and within the intracellular compartment (Lyons et al. 2001). ...
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Although the immune response has a prominent role in the pathophysiology of ulcerative colitis, sepsis, and systemic lupus erythematosus, a primary immune causation has not been established to explain the pathogenesis of these diseases. However, studies have reported significantly elevated levels of colonic epithelial hydrogen peroxide (a known colitic agent) in ulcerative colitis prior to the appearance of colitis. And patients with sepsis are reported to have toxic levels of blood hydrogen peroxide, whose pathologic effects mirror the laboratory and clinical abnormalities observed in sepsis. More recently, evidence supports a causal role for cellular hydrogen peroxide (a potent apoptotic agent) in the enhanced apoptosis believed to be the driving force behind auto-antigenic exposure and chronic immune activation in systemic lupus erythematosus. The different biological properties of hydrogen peroxide exert distinct pathologic effects depending on the site of accumulation within the body resulting in a unique disease patho-phenotype. On a cellular level, the build-up of hydrogen peroxide triggers apoptosis resulting in systemic lupus erythematosus, on a tissue level (colonic epithelium) excess hydrogen peroxide leads to inflammation and ulcerative colitis, and on a systemic level the pathologic effects of toxic concentrations of blood hydrogen peroxide result in bioenergetic failure and microangiopathic dysfunction leading to multiple organ failure and circulatory shock, characteristic of advanced sepsis. The aim of this paper is to provide a unified evidence-based common causal role for hydrogen peroxide in the pathogenesis of ulcerative colitis, sepsis, and systemic lupus erythematosus. Based on this new theory of pathogenesis, a novel evidence-based treatment of sepsis is also discussed.
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In this comprehensive evidence-based analysis of ulcerative colitis (UC), a causal role is identified for colonic epithelial hydrogen peroxide (H2O2) in both the pathogenesis and relapse of this debilitating inflammatory bowel disease. Studies have shown that H2O2 production is significantly increased in the non-inflamed colonic epithelium of individuals with UC. H2O2 is a powerful neutrophilic chemotactic agent that can diffuse through colonic epithelial cell membranes creating an interstitial chemotactic molecular "trail" that attracts adjacent intravascular neutrophils into the colonic epithelium leading to mucosal inflammation and UC. A novel therapy aimed at removing the inappropriate H2O2 mediated chemotactic signal has been highly effective in achieving complete histologic resolution of colitis in patients experiencing refractory disease with at least one (biopsy-proven) histologic remission lasting 14 years to date. The evidence implies that therapeutic intervention to prevent the re-establishment of a pathologic H2O2 mediated chemotactic signaling gradient will indefinitely preclude neutrophilic migration into the colonic epithelium constituting a functional cure for this disease. Cumulative data indicate that individuals with UC have normal immune systems and current treatment guidelines calling for the suppression of the immune response based on the belief that UC is caused by an underlying immune dysfunction are not supported by the evidence and may cause serious adverse effects. It is the aim of this paper to present experimental and clinical evidence that identifies H2O2 produced by the colonic epithelium as the causal agent in the pathogenesis of UC. A detailed explanation of a novel therapeutic intervention to normalize colonic H2O2, its rationale, components, and formulation is also provided.
The effect of X-ray radiation or antioxidants such as actinomycin D, cycloheximide and mitomycin C is studied on CHO, BHK and HeLa cells. X-ray radiation caused DNA single strand breaks (SSB) and double strand breaks (DSB) are prevented by cycloheximide and actionmycin-D. The DSB and SSB are significant in the case of X-ray radiation in combination with MMC, but different with actinomycin-D and cycloheximide in combination with X-ray radiation which causes less number of SSB and DSB. The ISC is observed more with X-ray radiation in combination with antioxidants mitomycin C (MMC) than that of cycloheximide and actinomycin-D, which individually causes inhibition of ISC induced by X-ray radiation. This observation proves that the MMC has an additive effect on X-ray induced ISC during cell proliferation. During cell proliferation, cell viability is observed with X-ray radiation and antioxidants which are dependent on the cell cycle phase. However, in the control cells, the initial Go-phase has shown negligible difference in per cent cell viability thereby during S-Phase gradual increase in the cell viability, and cell proliferation have been found to be stopped at G2 + M-Phase. On the contrary, cell viability and the extent of cell proliferation with X-ray radiation in combination with MMC have shown more damage (OH-damage) than is caused by X-ray radiation and MMC, separately. But, the fact is that actinomycin - D and cycloheximide act as antioxidants preventing thereby free radical formation and cell death, caused by X-ray radiation. During cell proliferation, cells observed from S and (G2 + M) phase exhibit difference in cell viability in all the treatments alone and in combination. HeLa cells have been found insensitive to X-ray radiation and could be ascribed to the presence of glutathoinc transferase, which is less in CHO/BHK cell line.
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