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因血色病中的慢性铁负荷能引起器官损伤，肾脏缺血再灌注时的损伤也与铁有关，因此我们评价了轻度亚急性铁负荷增加鼠脂质过氧化物及缺血性损害的敏感性。在实验组给雄性ＳＤ鼠腹内注射ｉｒｏｎｎｉｔｒｉｌｏｔｒｉａｃｅｔａｔｅ（Ｆｅ－ＮＴＡ）（ｌｍｇ／ｋｇ·ｄ，５ｄ），对照组鼠腹腔内注射媒介质ｎｉｔｒｉｌｏｔｒｉａｃｅ－ｔａｔｅ７２ｈ后鼠肾动脉缺血４０ｍｉｎ。铁负荷从基线增加２８％时血肌酐或组织学无任何改变。我们发现Ｆｅ－ＮＴＡ组左肾皮质ＭＤＡ量比ＮＴＡ组左肾皮质显著增加（Ｐ＜０．０１）。铁负荷组肾缺血２４ｈ、４８ｈ血肌酥显著高于对照组（３．３和３．４对２．２和０．８ｍｇ／ｄｌ），ＧＦＲ显著低于对照组（０．３对０．７８ｍｌ／ｍｉｎ）。利用半定量法评价铁负荷鼠肾组织学损害显示显著加重。
Because chronic iron overload in hemochromatosis can cause organ damage and renal ischemia-reperfusion injury is also iron-related, we evaluated the sensitivity of mild subacute iron overload to increased lipid peroxidation and ischemic damage in rats Sex. In the experimental group, male SD rats were injected intraperitoneally with ironnitrilotriacetate (Fe-NTA) (lmg / kg · d, 5d), and the control group was injected with nitrilotriacetat72h for 48 hours. There was no change in serum creatinine or histology with a 28% increase in iron load from baseline. We found that the amount of MDA in left renal cortex in Fe-NTA group was significantly higher than that in NTA group (P <0.01). Compared with control group (3.3 and 3.4 for 2.2 and 0.8 mg / dl), GFR was significantly lower in iron overload group than that in control group (0.3 vs 0.30). 78 ml / min). Semiquantitative evaluation of renal iron damage in renal tissue damage showed significant increase.