氯化鎘對小白鼠骨中鹼性和酸性磷酸酯解?之影響

Abstract

本實驗之目地在探討氯化鎘對小白鼠脛骨中鹼性和酸性磷酸酯解?及含鈣量間關係的影響。以ICR種系之雄性小白鼠(18-20g)為實驗材料，以0，200，300及400 μg/100g體重之氯化鎘作腹腔注射。然後每週犧牲小白鼠一批。本實驗顯示：在注射後第二週，骨中鹼性磷酸酯解?的活性即有顯著的降低（P<0.05），其降低之程度隨鎘劑量之增加及實驗時間之延長而更顯著。至第六週，三個實驗組(200，300，及400μg)骨中鹼性磷酸酯解?之活性分別為對照組者的76.9％，64.9％及55.7％，且其差異極為顯著（P<0.005）。骨中可溶性磷之含量亦隨鹼性磷酸酯解?之被抑制而減少。於第六週時，三個實驗組分別較對照組減少了31.7％，36.5％及41％（P<0.005）。酸性磷酸酯解?的活性與鹼性磷酸酯解?者正恰相反，其活性有增高的趨勢。至第六週時三個實驗組骨中該?之活性分別較對照組者增加了25％，35％及53.4％。同時可溶性鈣的含量亦隨之上升。在離體(In vitro)實驗中氯化鎘對骨中鹼性和酸性磷酸酯解?之影響，其結果與在活體(In vivo)者相吻合。脛骨中核醣核酸之合成在活體和離體實驗中均顯降低之現象。蛋白質之合成在活體實驗中有下降而離體實驗中卻無顯著差異。然經六週的實驗後，鎘在骨骼中的沈積量亦有顯著之增加。各實驗組較對照組分別增加了54％，74％及96％(P<0.005）。但鋅的含量卻遞減。從本研究結果顯示：當鹼性磷酸酯解?活性被抑制鋅的含量卻遞減。從本研究結果顯示：當鹼性磷酸酯解?活性被抑制，及酸性磷酸酯解?的活性上升時骨中鈣化反應受阻，同時骨骼呈現脫鈣現象。因此當動物受到長期鎘中毒時，就會造成骨骼嚴重的缺乏鈣質。

This reserach was aimed at investigating the in vivo and in vitro effects of CdCl2 on the alkaline and acid phosphatase (ALP and ACP) activity as well as the RNA and proteinsyntheses of the mice tibiae. The male mice of ICR strain were injected weekly intraperitoneally with three different dosage levels of CdCl2 varying from 200, 300 and 400 μg/100 g body wt.. The mice were sacrificed weekly after the injection. The activity of ALP was decreased (p<0.05) during the second week postinjection. By the 6th week, the activities of the ALP of the three experimental groups were 76.9%, 64.9% and 55.7% (p<0.005), when compared with the control. The concentration of soluble phosphorus of mouse tibia was also diminished. By the 6th week, the contents of the soluble phosphorus of the three experimental groups were 31.7%, 36.5% and 41% of the control. The activity of the ACP was contrary to that of the ALP's. CdCl2 had the tendency to elevate the activity of ACP, which increased 25%, 35% and 53.4% in the three experimental groups when compared with the control during the 6th week. Concurrently the concentrattion of the soluble calcium of the tibia was also augmented. The results of the in vitro experiments on ALP and ACP coincided with those of the in vivo ones. The biosynthesis of RNA was decreased both in the in vivo and in vitro experiments. However, the results of the in vitro experiments on the biosynthesis of protein did not confirm the in vivo results of decreased protein syntheses in the tibia due to CdCl2. During the six weeks of experimental interval, the deposition of cadmium in the mouse tibia increased significantly. The 200, 300 and 400 μg groups increase 54%, 74% and 96% respectively, when compared with the control. However, the content of zinc was reduced. The results showed that as the activity of the ALP was inhibited, and that of the ACP was elevated, the ossification in the tibia would be retarded and the decalcification would be accelerated. Consequently the long-term cadmium administration would make the bone lose calsium seriouly.