Fukuoka M, Niimi S, Zhou Y, Kobayashi T, Hayakawa T
Division of Biological Chemistry, National Institute of Health Sciences, Tokyo, Japan.
Biol Pharm Bull. 1996 Sep;19(9):1154-9. doi: 10.1248/bpb.19.1154.
We have reported that di-n-butyl phthalate (DBP) caused the depletion of circulating iron, characterized by the release of iron from both haemoglobin (Hb) and transferrin (Tf). The present study investigated whether the erythrocytes from DBP-treated rats were destroyed by nonparenchymal liver cells (NPC, including Kupffer cells) or spleen cells (SC). In the in vivo study, there were observed depletions of Hb in the blood and of iron in the hepatic Tf fraction, as well as an accumulation of iron in the hepatic hemosiderin (Hs) and splenic Tf fractions. In the in vitro study, mono-butyl phthalate (MBP), a metabolite of DBP, caused a depletion of iron in the plasma Tf, although a direct release of iron from Tf was not detectable. When erythrocytes from DBP-treated rats and erythrocytes preincubated with MBP both were incubated with NPC, respectively, the Hb was decomposed and the iron also accumulated in the cell debris. However, when the two kinds of erythrocytes were incubated with SC, respectively, no decomposition of Hb was observed at low and medium doses, but the highest dose induced an accumulation of iron to Tf. Therefore, the NPC may contribute in part to the decomposition of DBP- or MBP-affected erythrocytes.
我们曾报道邻苯二甲酸二正丁酯（DBP）会导致循环铁的消耗，其特征为血红蛋白（Hb）和转铁蛋白（Tf）中的铁释放。本研究调查了DBP处理大鼠的红细胞是否会被非实质肝细胞（NPC，包括库普弗细胞）或脾细胞（SC）破坏。在体内研究中，观察到血液中Hb减少，肝Tf部分中铁减少，以及肝含铁血黄素（Hs）和脾Tf部分中铁积累。在体外研究中，DBP的代谢产物单丁基邻苯二甲酸酯（MBP）导致血浆Tf中铁减少，尽管未检测到Tf中铁的直接释放。当分别将DBP处理大鼠的红细胞和预先与MBP孵育的红细胞与NPC一起孵育时，Hb分解，铁也在细胞碎片中积累。然而，当将这两种红细胞分别与SC孵育时，在低剂量和中剂量下未观察到Hb分解，但最高剂量诱导铁积累到Tf中。因此，NPC可能部分参与了受DBP或MBP影响红细胞的分解。
