人类先兆子痫毒血症、皮质静脉血栓形成和产后精神病患者的下丘脑地高辛和低镁血症

Ravi Kumar Kurup, Parameswara Achutha Kurup
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引用次数: 2

摘要

类异戊二烯途径产生三种关键代谢产物——地高辛(膜钠钾ATP酶抑制剂和神经递质转运调节剂)、多力酚(调节蛋白质的N-糖基化)和泛醌(自由基清除剂)。该途径在先兆子痫毒血症、皮质静脉血栓形成和产后精神病患者中进行了评估。它还被研究用于右半球、左半球和双半球优势患者的比较。研究结果表明,在所有三组患者中,类异戊二烯途径都随着地高辛合成的增加而上调。红细胞(RBC)膜Na+–K+ATP酶活性和血清镁水平也有所降低。血清色氨酸分解代谢产物增加,酪氨酸分解代谢产物减少。在所有三组中,随着血浆溶酶体酶的增加,血清dolichol和糖缀合物水平增加,溶酶体稳定性降低。血清泛醌水平较低,红细胞自由基参数升高。这些患者的红细胞膜胆固醇与磷脂的比例增加,膜中的糖结合物减少。这种模式与右半球占优势的模式相关。因此,类异戊二烯途径和下丘脑地高辛可能在CVT、PET和产后精神病的发病机制中发挥关键作用。J.Trace Elem。《实验医学》,2002年15:171–190。©2002 Wiley-Liss,股份有限公司。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Hypothalamic digoxin and hypomagnesemia in human pre-eclampsic toxemia, cortical venous thrombosis, and postpartum psychosis
The isoprenoid pathway produces three key metabolites—digoxin (membrane sodium-potassium ATPase inhibitor and regulator of neurotransmitter transport), dolichol (regulates N-glycosylation of proteins), and ubiquinone (free radical scavenger). The pathway was assessed in patients with pre-eclampsic toxaemia, cortical venous thrombosis, and postpartum psychosis. It was also studied for comparison in patients with right hemispheric, left hemispheric, and bihemispheric dominance. The results of the study showed that the isoprenoid pathway was upregulated with increased digoxin synthesis in all the three groups of patients. There was also a reduction in red blood cell (RBC) membrane Na+–K+ ATPase activity and serum magnesium levels. There was an increase in serum tryptophan catabolites and reduction in tyrosine catabolites. The serum dolichol and glycoconjugate levels were increased and lysosomal stability reduced with increased plasma lysosomal enzymes in all the three groups. The serum ubiquinone levels were low, and RBC free radical parameters increased. The RBC membrane cholesterol: phospholipid ratio was increased, and glycoconjugate was reduced in the membrane of these patients. This pattern correlated with those in right hemispheric dominance. The isoprenoid pathway and hypothalamic digoxin may thus play a crucial role in the pathogenesis of CVT, PET, and postpartum psychosis. J. Trace Elem. Exp. Med. 15:171–190 2002. © 2002 Wiley-Liss, Inc.
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