期刊
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
卷 23, 期 1-3, 页码 191-198出版社
KARGER
DOI: 10.1159/000204107
关键词
Malaria; Cell volume; Phosphatidylserine; Apoptosis; Cell death; Eryptosis; Taxol; Docetaxel
资金
- Deutsche Forschungsgemeinschaft [La 315/6-1, La 315/13-1, Hu 781/4-3]
Paclitaxel triggers suicidal erythrocyte death or eryptosis, characterized by exposure of phosphatidylserine at the erythrocyte surface and cell shrinkage. Eryptosis of infected erythrocytes may delay development of parasitemia and thus favourably influence the course of malaria. The present study explored whether paclitaxel influences in vitro parasite growth and eryptosis of Plasmodium falciparum infected human erythrocytes and in vivo parasitemia and survival of Plasmodium berghei infected mice. Phosphatidylserine exposing erythrocytes were identified utilizing annexin V binding and erythrocyte volume was estimated from forward scatter in FACS analysis. In vitro infection of human erythrocytes with P. falciparum increased annexin binding and decreased forward scatter, effects augmented in the presence of paclitaxel (>= 0.01 mu M). Paclitaxel (>= 0.01 mu M) significantly decreased intraerythrocytic DNA/RNA content and in vitro parasitemia. In Plasmodium berghei infected mice parasitemia was significantly decreased (from 55.8% to 28.6% of circulating erythrocytes 20 days after infection) and mouse survival significantly enhanced (from 0% to 69.23% 25 days after infection) by administration of 8.5 mg/kg.b.w. of paclitaxel intraperitoneally from the eighth day of infection. In conclusion, paclitaxel decreases parasitemia and enhances survival of P. berghei infected mice, an effect, which may be due to stimulation of eryptosis and/or a direct toxic effect on the parasite. Copyright (C) 2009 S. Karger AG, Basel
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据