Antoni F, Csuka I, Hrabák A, Temesi A, Szende B, Lapis K
1st Institute of Biochemistry, Semmelweis University of Medical School, Budapest, Hungary.
Acta Biochim Biophys Hung. 1989;24(4):299-311.
Murine peritoneal macrophages were treated in vitro with L-leucine methyl ester (0.25-5.0 mM). This treatment resulted in an inhibition of the amino acid incorporation into the cells both at 4 degrees C and 37 degrees C during a relatively short incubation period. The adherence of macrophages was not changed by the treatment. Bacterial phagocytosis was partly influenced: Leu-OMe did not change the binding but the engulfment of opsonized bacteria was blocked. Damage of the plasma membrane caused by Leu-OMe was not so serious as that produced by specific anti-PEC antiserum. Leu-OMe is a lysosomotropic agent accumulated preferentially by lysosomes. The vacuolization of the cells and the dilatation of the vacuoles are evidences for the intracellular damage. In the early phase this damage is characterized only by the leakage of the cytoplasm, later the damage of the plasma membrane can also be demonstrated.
用L-亮氨酸甲酯(0.25 - 5.0 mM)对小鼠腹膜巨噬细胞进行体外处理。在相对较短的孵育期内,这种处理导致在4℃和37℃下氨基酸掺入细胞的过程均受到抑制。巨噬细胞的黏附未因该处理而改变。细菌吞噬作用受到部分影响:亮氨酸甲酯未改变调理素化细菌的结合,但阻止了其吞噬。亮氨酸甲酯引起的质膜损伤不如特异性抗PEC抗血清产生的损伤严重。亮氨酸甲酯是一种溶酶体亲和剂,优先被溶酶体积累。细胞空泡化和液泡扩张是细胞内损伤的证据。在早期阶段,这种损伤仅表现为细胞质渗漏,后期也可证明质膜受损。