Balázs A
Haematologia (Budap). 1976;10(3-4):433-44.
The ultrastructural effects of the endogenous inhibitor, granuloid crude extract (GCE), known to control the proliferation of myeloid cells, and of the current hexitol derivative, 1,2 : 5,6-dianhydrogalactitol (DAD) were compared on the rat bone marrow. A single intraperitoneally injected LD50 dose of DAD induces the following changes in the fine structure: The mitochondria become swollen, the matrix less electron-dense, the cristae fragmentate, the ribosomes aggregate, anomalies appear in the perinuclear the cell membranes, and myelin figures and intranuclear bodies develop. Autophagy, degeneration and the phagocytotic activity of the reticulum cells is appreciable in 4 hours after treatment and increase by the 24th hour. The toxic effect of DAD is cell aspecific but in the ultrastructure its myelotropic effect manifests earlier than in erythropoiesis. In contrast, the arrest caused by a single dose of the endogenous granuloid inhibitor [2] is cell-specific and non-toxic.
已知内源性抑制剂粒状粗提取物(GCE)可控制髓细胞增殖,将其与目前的己糖醇衍生物1,2:5,6 - 脱水半乳糖醇(DAD)对大鼠骨髓的超微结构影响进行了比较。单次腹腔注射DAD的半数致死剂量会在精细结构上引起以下变化:线粒体肿胀,基质电子密度降低,嵴断裂,核糖体聚集,核周细胞膜出现异常,髓鞘样结构和核内小体形成。治疗后4小时,网状细胞的自噬、变性和吞噬活性明显,到第24小时增加。DAD的毒性作用是非细胞特异性的,但在超微结构上其对髓细胞的作用比在红细胞生成中表现得更早。相比之下,单剂量内源性粒状抑制剂[2]引起的停滞是细胞特异性且无毒的。