Eiselt Jaromír, Racek Jaroslav, Opatrný Karel, Trefil Ladislav, Stehlík Pavel
Department of Medicine I, Charles University, Medical School and Teaching Hospital Pilsen, Pilsen, Czech Republic.
Blood Purif. 2006;24(5-6):531-7. doi: 10.1159/000096474. Epub 2006 Oct 23.
BACKGROUND/AIMS: Vitamin C levels decrease during hemodialysis (HD), which deteriorates antioxidant defense. Vitamin C may also act pro-oxidatively, via reduction in Fe(III). We sought to determine whether intravenous iron (Fe(iv))-induced oxidative stress differs in HD patients with low and physiological vitamin C levels and whether intravenous vitamin C (C(iv)) administration during HD would change the response to Fe(iv).
Twenty patients with vitamin C deficiency (median 15.7 micromol/l, range 8.0-22.7) received Fe(iv) (100 mg iron sucrose between 150 and 180 min of HD). After 4 weeks of oral supplementation, the levels of vitamin C were comparable with those of controls (60.1 micromol/l, range 47.4-70.9). Patients were subsequently treated with (1) Fe(iv), (2) Fe(iv) and continuous 2 mg/min C(iv) throughout HD, (3) saline (S), and (4) S+C(iv). Plasma thiobarbituric acid reacting substances (TBARS) and vitamin C were assessed before, during and after FE(iv)(S), and 15, 30 and 60 min after infusion.
Fe(iv) induced a comparable rise in TBARS in patients with vitamin C deficiency (before Fe(iv), 1.9 micromol/l, range 1.4-1.9; after Fe(iv), 2.6 micromol/l, range 2.3-2.9; p < 0.01) and in those with normal vitamin C (before Fe(iv), 1.9 micromol/l, range 1.7-2.1; after Fe(iv), 2.6 micromol/l, range 2.5-2.9; p < 0.01). Fe(iv)+C(iv) resulted in a greater increase in TBARS (after Fe(iv), 3.1 micromol/l, range 2.8-3.2) compared with Fe(iv) (p < 0.01).
Iron sucrose-induced oxidative stress is comparable in HD patients with vitamin C deficiency and in those with normal vitamin C. We documented a pro-oxidative effect of vitamin C during Fe(iv)+C(iv) administration.
背景/目的:血液透析(HD)期间维生素C水平会降低,这会削弱抗氧化防御能力。维生素C也可能通过还原Fe(III)而发挥促氧化作用。我们试图确定静脉注射铁(Fe(iv))诱导的氧化应激在维生素C水平低和正常的HD患者中是否存在差异,以及HD期间静脉注射维生素C(C(iv))是否会改变对Fe(iv)的反应。
20例维生素C缺乏患者(中位数15.7微摩尔/升,范围8.0 - 22.7)在HD的150至180分钟期间接受Fe(iv)(100毫克蔗糖铁)。口服补充4周后,维生素C水平与对照组相当(60.1微摩尔/升,范围47.4 - 70.9)。患者随后接受以下治疗:(1)Fe(iv),(2)HD期间全程持续2毫克/分钟的C(iv)和Fe(iv),(3)生理盐水(S),以及(4)S + C(iv)。在Fe(iv)(S)之前、期间和之后以及输注后15、30和60分钟评估血浆硫代巴比妥酸反应物质(TBARS)和维生素C。
维生素C缺乏患者(Fe(iv)之前,1.9微摩尔/升,范围1.4 - 1.9;Fe(iv)之后,2.6微摩尔/升,范围2.3 - 2.9;p < 0.01)和维生素C正常的患者(Fe(iv)之前,1.9微摩尔/升,范围1.7 - 2.1;Fe(iv)之后,2.6微摩尔/升,范围2.5 - 2.9;p < 0.01)中,Fe(iv)诱导的TBARS升高相当。与Fe(iv)相比,Fe(iv)+ C(iv)导致TBARS升高幅度更大(Fe(iv)之后,3.1微摩尔/升,范围2.8 - 3.2)(p < 0.01)。
蔗糖铁诱导的氧化应激在维生素C缺乏的HD患者和维生素C正常的患者中相当。我们记录了在Fe(iv)+ C(iv)给药期间维生素C的促氧化作用。