Ayala A, Kierszenbaum F
Mol Biochem Parasitol. 1987 Feb;23(1):63-9. doi: 10.1016/0166-6851(87)90188-5.
Treatment of Trypanosoma cruzi blood trypomastigotes with p-chloromercuriphenylsulfonic acid (PCMS) increased the association of the parasite with either mouse resident peritoneal macrophages or rat heart myoblasts in vitro. The effect was evidenced by elevation of both the percentage of host cells with parasites and the number of flagellates per 100 cells. The effect of PCMS appeared to be largely on the process of parasite penetration rather than surface binding as it was seen at 37 degrees C but not at 4 degrees C. A short pretreatment time, 5 min, was sufficient to elicit the enhancement, suggesting that the primary effect of PCMS might be at the parasite's cell surface. The PCMS effect was reversible as the parasite returned to normal levels of association with the host cells in less than 4 h after removal of excess PCMS. That sulfhydryl groups were involved in the PCMS effect was indicated by the abilities of excess cysteine and glutathione to block it. These results suggest a role for free sulfhydryl groups on the parasite surface in the process of host cell invasion.
用对氯汞苯磺酸(PCMS)处理克氏锥虫血液型锥鞭毛体,可增强该寄生虫在体外与小鼠常驻腹膜巨噬细胞或大鼠心脏成肌细胞的结合。宿主细胞携带寄生虫的百分比以及每100个细胞中鞭毛虫的数量增加,证明了这种作用。PCMS的作用似乎主要体现在寄生虫的侵入过程而非表面结合,因为在37℃时可见这种作用,而在4℃时则不然。短时间预处理5分钟就足以引发这种增强作用,这表明PCMS的主要作用可能发生在寄生虫的细胞表面。PCMS的作用是可逆的,因为在去除过量的PCMS后不到4小时,寄生虫与宿主细胞的结合就恢复到了正常水平。过量的半胱氨酸和谷胱甘肽能够阻断PCMS的作用,这表明巯基参与了PCMS的作用。这些结果表明,寄生虫表面的游离巯基在宿主细胞入侵过程中发挥了作用。