Sarkar M, Mookerjea S
Biochem J. 1985 Apr 15;227(2):675-82. doi: 10.1042/bj2270675.
Hepatocytes were prepared from control and inflamed rats. The incorporation of [14C]mannose into protein was increased in inflamed compared with control hepatocytes. The incorporation of [14C]mannose into protein was also increased when the hepatocytes were cultured in presence of dexamethasone (1 microM), either from control or inflamed rats. At the same time the incorporation of [14C]mannose into dolichol phosphate mannose and dolichol-linked oligosaccharide was increased due to inflammation. The presence of dexamethasone in the hepatocyte culture caused an increased formation of these two products; in particular its effect on oligosaccharide lipid formation was very pronounced. The ratios of activities of formation of [14C]mannose-labelled oligosaccharide lipid in inflamed over control hepatocytes gradually decrease when increasing amounts of exogenous dolichol phosphate was added in cell homogenate assay mixture. These results suggest that the increase of oligosaccharide lipid formation in inflammation could be due to a higher concentration of endogenous dolichol phosphate, as was shown for dolichol phosphate mannose formation in inflammation [Sarkar & Mookerjea (1984) Biochem. J. 219, 429-436]. In contrast, the ratio of activities of [14C]mannose-labelled oligosaccharide lipid between dexamethasone-treated and untreated hepatocytes shows only a slight increase when increasing concentrations of exogenous dolichol phosphate were added to the assays. This suggests that the stimulation of dolichol pyrophosphate oligosaccharide synthesis observed in dexamethasone treatment is probably due to the higher level of enzymes involved in oligosaccharide synthesis rather than higher level of endogenous dolichol phosphate in these cells.
从对照大鼠和炎症大鼠中分离制备肝细胞。与对照肝细胞相比,炎症肝细胞中[14C]甘露糖掺入蛋白质的量增加。当对照或炎症大鼠的肝细胞在存在地塞米松(1 microM)的情况下培养时,[14C]甘露糖掺入蛋白质的量也会增加。同时,由于炎症,[14C]甘露糖掺入磷酸多萜醇甘露糖和多萜醇连接的寡糖的量增加。肝细胞培养中地塞米松的存在导致这两种产物的形成增加;特别是其对寡糖脂形成的影响非常显著。在细胞匀浆测定混合物中加入越来越多的外源磷酸多萜醇时,炎症肝细胞中[14C]甘露糖标记的寡糖脂形成活性与对照肝细胞的比值逐渐降低。这些结果表明,炎症中寡糖脂形成的增加可能是由于内源性磷酸多萜醇浓度较高,正如炎症中磷酸多萜醇甘露糖形成的情况所示[Sarkar & Mookerjea (1984) Biochem. J. 219, 429 - 436]。相反,当向测定中加入越来越高浓度的外源磷酸多萜醇时,地塞米松处理的肝细胞与未处理的肝细胞之间[14C]甘露糖标记的寡糖脂活性比值仅略有增加。这表明在地塞米松处理中观察到的焦磷酸多萜醇寡糖合成的刺激可能是由于这些细胞中参与寡糖合成的酶水平较高,而不是内源性磷酸多萜醇水平较高。