Modification of iron uptake and lipid peroxidation by hypoxia, ascorbic acid, and alpha-tocopherol in iron-loaded rat myocardial cell cultures.
Modification of iron uptake and lipid peroxidation by hypoxia, ascorbic acid, and alpha-tocopherol in iron-loaded rat myocardial cell cultures.
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发表时间：
1987-09
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通讯作者：
C. Hershko;G. Link;A. Pinson
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作者：
C. Hershko;G. Link;A. Pinson
抗坏血酸，α-生育酚，和缺氧的能力，以修改铁的吸收，螯合，和毒性所表现的生成丙二醛（MDA）的研究在心肌细胞培养获得的新生大鼠。在无血清Ham F-10培养基中暴露于以59 Fe-柠檬酸铁铵形式提供的20微克/ml铁导致24小时内39%的铁积累和细胞MDA增加10至12倍。缺氧（1%氧）导致铁的摄取增加了两倍以上，但细胞MDA浓度只有微小的变化。抗坏血酸和α-生育酚（1毫克/毫升）对铁的吸收和MDA的产生有相反的影响。抗坏血酸使24小时铁吸收减少73%（P <0.001），而α-生育酚使铁吸收增加19%（P <0.025）。与此相反，铁负荷后的细胞MDA增加了86%的抗坏血酸，并减少了75%的α-生育酚（P小于0.001）。细胞MDA相对于铁摄取百分比的增加比率（脂质过氧化比率）为7.29（铁负荷加抗坏血酸）与0.13（铁负荷加α-生育酚），两个极端之间的差异为56倍。在体外去铁胺治疗3小时导致铁负载的心脏细胞的放射性铁含量减少53%，MDA减少40%。同时去铁胺和抗坏血酸或α-生育酚治疗不影响铁动员，但对MDA浓度有深远的影响。抗坏血酸完全阻止去铁胺对铁负载细胞中MDA浓度的有益作用，而α-生育酚增强去铁胺的作用。（250字处删节）
The ability of ascorbic acid, alpha-tocopherol, and hypoxia to modify iron uptake, chelation, and toxicity as manifested by the generation of malonyldialdehyde (MDA) was studied in myocardial cell cultures obtained from newborn rats. Exposure to 20 micrograms/ml iron provided as 59Fe-ferric ammonium citrate in serum-free Ham F-10 culture medium resulted in the accumulation of 39% of the iron within 24 hours and a 10- to 12-fold increase in cellular MDA. Hypoxia (1% oxygen) resulted in a more than twofold increase in iron uptake but only minor changes in cellular MDA concentrations. Ascorbic acid and alpha-tocopherol (1 mg/ml) had opposing effects on iron uptake and MDA production. Ascorbic acid reduced 24-hour iron uptake by 73% (P less than 0.001) whereas alpha-tocopherol increased iron uptake by 19% (P less than 0.025). In contrast, cellular MDA after iron loading increased by 86% with the addition of ascorbate, and was reduced by 75% with alpha-tocopherol (P less than 0.001). The ratio of increase in cellular MDA relative to percent iron uptake (lipid peroxidation ratio) was 7.29 with iron loading plus ascorbate vs. 0.13 with iron loading plus alpha-tocopherol, a 56-fold difference between the two extremes. In vitro deferoxamine treatment for 3 hours resulted in a 53% reduction in the radioactive iron content of iron-loaded heart cells and a 40% reduction in MDA. Simultaneous deferoxamine and ascorbate or alpha-tocopherol treatment did not affect iron mobilization, but had a profound effect on MDA concentrations. Ascorbic acid prevented entirely the beneficial effect of deferoxamine on MDA concentrations in iron-loaded cells, whereas alpha-tocopherol potentiated the effect of deferoxamine.(ABSTRACT TRUNCATED AT 250 WORDS)