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[单次照射后0-(β-羟乙基)-芸香苷对大鼠脑抗水肿及辐射防护作用的组织化学与超微结构研究。2. 碳水化合物代谢及酸性磷酸酶激活的组织化学研究]

[Histochemical and ultrastructural studies on anti-edematous and radiation-protective action of 0-(beta-hydroxyethyl)-rutosides on the rat brain after single irradiation. 2. Histochemical study on carbohydrate metabolism and acid phosphatase activation].

作者信息

Thiel H J, Lierse W, Lehmann F M, Sauer R

机构信息

Strahlentherapeutische Klinik und Poliklinik der Universität Erlangen-Nürnberg.

出版信息

Strahlenther Onkol. 1988 Nov;164(11):662-73.

PMID:3201383
Abstract

The disturbances of the carbohydrate metabolism and the activation of acid phosphatases with and without protection by O-(beta-hydroxyethyl)-rutoside (HR) were studied in irradiated rat brains by means of the light microscope. The histochemically demonstrable deposition of glycogen and acid mucopolysaccharides serves as a criterion for a reversible lesion of the irradiated cerebral tissue. The extent of local activation of repair processes following to irradiation can be determined by the quantity of acid phosphatases in the lysosomes. For the dose range of 1 to 5 Gy, HR seems to exert a protective effect on the cellular metabolism of the irradiated cerebral tissue shown by a slight decrease of glycogen and mucopolysaccharide deposits compared to the untreated animals. However, when exceeding a threshold dose of 10 Gy, the deposition of carbohydrates in the HR group is strongly increased. A slightly increased activity of acid phosphatases induced by HR can be supposed at best for the dose range of 5 to 7.5 Gy. If the dose is even more increased, the reverse effect found in the carbohydrate metabolism, too, and an increased activation of acid phosphatases in the control group will be observed. This unexpected reversion of the protective effect could be related to the assumed inhibitory effect of HR on the ATPases and thus on the anaerobic part of glycolysis or to a breakdown of the cell interaction system of endothelial cells, glia cells, and neurons.

摘要

利用光学显微镜研究了照射大鼠脑内碳水化合物代谢紊乱以及在有和没有O-(β-羟乙基)-芦丁(HR)保护的情况下酸性磷酸酶的激活情况。糖原和酸性粘多糖的组织化学可显示沉积作为照射脑组织可逆性损伤的一个标准。照射后修复过程的局部激活程度可通过溶酶体中酸性磷酸酶的量来确定。对于1至5 Gy的剂量范围,与未处理的动物相比,HR似乎对照射脑组织的细胞代谢发挥保护作用,表现为糖原和粘多糖沉积略有减少。然而,当超过10 Gy的阈值剂量时,HR组中碳水化合物的沉积会大幅增加。对于5至7.5 Gy的剂量范围,最多只能推测HR会引起酸性磷酸酶活性略有增加。如果剂量进一步增加,在碳水化合物代谢中也会发现相反的效果,并且会观察到对照组中酸性磷酸酶的激活增加。这种保护作用的意外逆转可能与HR对ATP酶进而对糖酵解的厌氧部分的假定抑制作用有关,或者与内皮细胞、神经胶质细胞和神经元的细胞相互作用系统的破坏有关。

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