Günther T, Gossrau R, Vormann J, Höllriegl V, Graf R
Institute of Molecular Biology and Biochemistry, Free University of Berlin, FRG.
Biol Trace Elem Res. 1988 Dec;18:49-58. doi: 10.1007/BF02917488.
Nonhemoglobin Fe (non Hb-Fe) content in fetal serum and liver is much higher than in maternal serum and liver. After feeding a Zn-deficient diet to pregnant rats from d 0 to 21, non Hb-Fe content in maternal and fetal serum and liver was increased. After oral application of salicylic acid (300 mg/kg) from d 16 to 20 to normally fed and Zn-deficient dams, non Hb-Fe content in maternal and particularly in fetal serum and liver was drastically increased. In the kidney, Fe was accumulated to a small amount resulting from Zn deficiency and salicylate treatment. Fe accumulation in the liver occurred in all cell fractions, particularly in microsomes. Fe accumulation was confirmed and extended histochemically by Prussian blue staining. It is assumed that salicylate increases intestinal Fe resorption and fetal transfer of Fe. It is discussed that salicylate nephrotoxicity and its enhancement by Zn deficiency is not caused by an Fe-dependent mechanism.
胎儿血清和肝脏中的非血红蛋白铁(非Hb-Fe)含量远高于母体血清和肝脏中的含量。从第0天到第21天给怀孕大鼠喂食缺锌饮食后,母体和胎儿血清及肝脏中的非Hb-Fe含量增加。从第16天到第20天给正常喂养和缺锌的母鼠口服水杨酸(300mg/kg)后,母体尤其是胎儿血清和肝脏中的非Hb-Fe含量急剧增加。在肾脏中,由于缺锌和水杨酸盐处理,铁有少量积累。肝脏中的铁积累发生在所有细胞组分中,尤其是微粒体。通过普鲁士蓝染色在组织化学上证实并扩展了铁积累。推测水杨酸盐可增加肠道铁吸收和铁向胎儿的转运。讨论了水杨酸盐肾毒性及其因缺锌而增强并非由铁依赖性机制引起。