The oxidants hypochlorite and hydrogen peroxide induce distinct patterns of acute lung injury

IF 4.2 2区生物学 Q2 BIOCHEMISTRY & MOLECULAR BIOLOGY

Biochimica et biophysica acta. Molecular basis of disease Pub Date : 2004-11-05 DOI:10.1016/j.bbadis.2004.07.003

Stefan Hammerschmidt , Hans Wahn

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Abstract

Oxidative stress due to activated neutrophils, macrophages and endothelial cells plays a crucial role in acute lung injury. This study compares the effects of the nonradical oxidants hypochlorite (HOCl) and hydrogen peroxide (H₂O₂) on pulmonary artery pressure [PAP (torr)], capillary filtration coefficient (K_f,c), tissue lipid peroxidation (LPO) and reduced glutathione (GSH) depletion. HOCl, H₂O₂ (1000 nmol min⁻¹) or buffer (control) is infused into isolated rabbit lungs. PAP, K_f,c and lung weight were measured. Experiments were terminated after 105 min or when fluid retention exceeded 50 g. Lung tissue was analyzed for LPO products and GSH. The oxidants induced comparable maximum effects. However, the patterns of lung injury were distinct: H₂O₂ infusion evoked an early biphasic pressure response (ΔPAP_max 2.8±0.22/4.2±0.37 after 5.7±1.4/39±4.0 min) and a sixfold increase in K_f,c after 90 min. HOCl application caused a late pressure response (ΔPAP_max 7.6±1.7 after 50.6±3.7 min) and a sevenfold increase in K_f,c after 60 min. H₂O₂-induced effects were attenuated by desferal. This may suggest an involvement of transition metal catalysed hydroxyl radical formation. Different oxidants induced distinct patterns of changes in PAP and K_f,c, which are accompanied by a comparable accumulation of LPO products and by a distinct degree of GSH depletion.

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氧化剂次氯酸盐和过氧化氢诱导急性肺损伤的不同模式。

由活化的中性粒细胞、巨噬细胞和内皮细胞引起的氧化应激在急性肺损伤中起重要作用。本研究比较了非自由基氧化剂次氯酸盐(HOCl)和过氧化氢(H2O2)对肺动脉压[PAPtorr]、毛细血管过滤系数(Kf,c)、组织脂质过氧化(LPO)和还原性谷胱甘肽(GSH)消耗的影响。将HOCl、H2O2 (1000 nmol min(-1))或缓冲液(对照)注入离体兔肺。测定PAP、K(f,c)和肺质量。实验在105min后或当液体潴留超过50g时终止。分析肺组织中LPO产物和谷胱甘肽。氧化剂引起了类似的最大效应。然而，肺损伤的模式是不同的:H2O2输注引起早期双相压力反应(5.7+/-1.4/39+/-4.0 min后DeltaPAPmax为2.8+/-0.22/4.2+/-0.37)，90 min后Kf,c增加6倍。HOCl应用引起晚期压力反应(50.6+/-3.7 min后DeltaPAPmax为7.6+/-1.7)，60 min后Kf,c增加7倍。H2O2诱导的效应因延迟而减弱。这可能暗示了过渡金属催化羟基自由基形成的参与。不同的氧化剂诱导不同模式的PAP和Kf,c的变化，这伴随着相当的LPO产物积累和不同程度的谷胱甘肽消耗。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

Biochimica et biophysica acta. Molecular basis of disease 生物-生化与分子生物学

CiteScore

12.30

自引率

0.00%

发文量

218

审稿时长

32 days

期刊介绍： BBA Molecular Basis of Disease addresses the biochemistry and molecular genetics of disease processes and models of human disease. This journal covers aspects of aging, cancer, metabolic-, neurological-, and immunological-based disease. Manuscripts focused on using animal models to elucidate biochemical and mechanistic insight in each of these conditions, are particularly encouraged. Manuscripts should emphasize the underlying mechanisms of disease pathways and provide novel contributions to the understanding and/or treatment of these disorders. Highly descriptive and method development submissions may be declined without full review. The submission of uninvited reviews to BBA - Molecular Basis of Disease is strongly discouraged, and any such uninvited review should be accompanied by a coverletter outlining the compelling reasons why the review should be considered.