Hamori C J, Lasic D D, Vreman H J, Stevenson D K
University of California, San Diego, School of Medicine, La Jolla 92037.
Pediatr Res. 1993 Jul;34(1):1-5. doi: 10.1203/00006450-199307000-00001.
Metalloporphyrin inhibitors of heme oxygenase have been studied for use in the prevention of hyperbilirubinemia of the neonate. One report has suggested that incorporation of these drugs into liposomes can increase their localization to the spleen, dramatically reducing heme oxygenase activity in that important heme-degrading organ. We sought to further increase porphyrin delivery to the spleen by using reticuloendothelial blockade with blank liposomes 2 h before injection of 0.3 microns extruded zinc protoporphyrin liposomes (L-ZnPP). Control adult rats without hemolysis had splenic heme oxygenase activity of 1.07 +/- 0.09 nmol carbon monoxide (CO)/h/mg protein. Rats treated with L-ZnPP alone had splenic heme oxygenase activity of 0.53 +/- 0.16 nmol CO/h/mg protein 6 h after L-ZnPP dosing. However, rats treated with 1000 mumol of blank liposomes per kg to saturate the reticuloendothelial system 2 h before L-ZnPP administration had splenic heme oxygenase activity of 0.25 +/- 0.16 nmol CO/h/mg protein at t = 6 h, which is significantly less than that of the L-ZnPP alone group (p < 0.05). In adult rats treated with heat-damaged red blood cells (RBC) to simulate hemolysis, treatment with 10 mumol of aqueous ZnPP per kg or 10 mumol of untargeted L-ZnPP per kg did not produce a difference from control in total body bilirubin production as estimated by CO excretion. However, RBC-treated rats given 1000 mumol of blank liposomes per kg 2 h before L-ZnPP administration produced significantly less CO than control, aqueous ZnPP-treated, and untargeted L-ZnPP-treated rats from 8 to 12 h after RBC treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
血红素加氧酶的金属卟啉抑制剂已被研究用于预防新生儿高胆红素血症。一份报告表明,将这些药物包封于脂质体中可增加其在脾脏中的定位,显著降低该重要血红素降解器官中的血红素加氧酶活性。我们试图通过在注射0.3微米挤压的锌原卟啉脂质体(L-ZnPP)前2小时用空白脂质体进行网状内皮系统阻断,进一步增加卟啉向脾脏的递送。未发生溶血的对照成年大鼠脾脏血红素加氧酶活性为1.07±0.09 nmol一氧化碳(CO)/小时/毫克蛋白。单独给予L-ZnPP的大鼠在给予L-ZnPP 6小时后脾脏血红素加氧酶活性为0.53±0.16 nmol CO/小时/毫克蛋白。然而,在给予L-ZnPP前2小时用每千克1000 μmol空白脂质体使网状内皮系统饱和的大鼠,在t = 6小时时脾脏血红素加氧酶活性为0.25±0.16 nmol CO/小时/毫克蛋白,显著低于单独给予L-ZnPP组(p < 0.05)。在用热损伤红细胞(RBC)处理以模拟溶血的成年大鼠中,每千克给予10 μmol水相ZnPP或每千克10 μmol非靶向L-ZnPP处理,根据CO排泄估计的全身胆红素生成与对照相比无差异。然而,在给予L-ZnPP前2小时每千克给予1000 μmol空白脂质体的RBC处理大鼠,在RBC处理后8至12小时产生的CO明显少于对照、水相ZnPP处理和非靶向L-ZnPP处理的大鼠。(摘要截短于250字)