Lehmann F M, Lierse W, Thiel H J
Abteilung für Neuroanatomie, Anatomisches Institut der Universität Hamburg, BRD.
Acta Anat (Basel). 1989;135(3):275-80. doi: 10.1159/000146767.
X-ray-induced tissue damage in the brain of adult rats was investigated in the presence or absence of O-(beta-hydroxyethyl)-rutosides (OHR; active agents of Venoruton, Zyma-Blaes, München, FRG). Histochemical methods were used for the detection of glycogen (periodic acid-Schiff), acid mucopolysaccharides (Hale) and acid phosphatases (Gomori) by light microscopy. The tissue alterations were reduced after drug application in the dose range between 5 and 7.5 Gy (300 kV, 12 mA). Exposure of the animals to higher irradiation doses (10, 20 Gy) led to an inversion of the drug effect, now exerting pronounced tissue injury. For a possible explanation we discuss the inhibitory influence of rutosides (e.g. OHR) on the glycolytic pathway. Hence, a vital energy source of brain tissue could be impaired by the drug after reaching a threshold of 10 Gy.
在成年大鼠脑部存在或不存在O-(β-羟乙基)芦丁（OHR；维脑路通、德国慕尼黑Zyma-Blaes的活性剂）的情况下，研究了X射线诱导的组织损伤。通过光学显微镜，使用组织化学方法检测糖原（过碘酸-希夫反应）、酸性粘多糖（黑尔反应）和酸性磷酸酶（戈莫里反应）。在5至7.5 Gy（300 kV，12 mA）的剂量范围内给药后，组织改变有所减轻。动物暴露于更高的辐射剂量（10、20 Gy）导致药物作用反转，此时会造成明显的组织损伤。为了给出可能的解释，我们讨论了芦丁（如OHR）对糖酵解途径的抑制作用。因此，在达到10 Gy的阈值后，该药物可能会损害脑组织的重要能量来源。
