约氏疟原虫感染对小鼠脑γ-氨基丁酸代谢的影响。

Effect of Plasmodium yoelii infection on GABA metabolism of mouse brain.

作者信息

Sharma M C, Tripathi L M, Dutta G P, Sagar P, Pandey V C

机构信息

Division of Biochemistry, Central Drug Research Institute, Lucknow, India.

出版信息

Exp Mol Pathol. 1990 Apr;52(2):243-8. doi: 10.1016/0014-4800(90)90009-3.

DOI:10.1016/0014-4800(90)90009-3

PMID:2332040

Abstract

Plasmodium yoelii infection in albino mice decreased the activity of brain glutamic acid decarboxylase (GAD) by about 30 and 48% in crude homogenate and its synaptosomal fraction, respectively. The decrease was evident from 20% parasitemia and remained more or less constant up to 80% parasitemia. The Km values of GAD in normal and infected animals were 1.2 x 10(-2) and 3.3 x 10(-2) mM, respectively, indicating a decrease in enzyme substrate affinity due to infection. The lowered GAD activity rose to slightly above normal by treatment of infected animals with chloroquine. Decrease in GAD activity reflected lower gamma-aminobutyric acid (GABA) levels in the infected brain; however, GABA-transaminase activity was not significantly influenced by infection. It has been proposed that impaired GABA synthesis may be due to hypoxia induced by malarial infection.

摘要

约氏疟原虫感染白化小鼠后，其粗匀浆和突触体部分中脑谷氨酸脱羧酶（GAD）的活性分别降低了约30%和48%。从20%的寄生虫血症开始，这种降低就很明显，并且在高达80%的寄生虫血症时或多或少保持恒定。正常动物和感染动物中GAD的Km值分别为1.2×10⁻²和3.3×10⁻² mM，表明感染导致酶与底物的亲和力降低。用氯喹治疗感染动物后，降低的GAD活性略有上升至略高于正常水平。GAD活性的降低反映了感染大脑中γ-氨基丁酸（GABA）水平的降低；然而，GABA转氨酶活性并未受到感染的显著影响。有人提出，GABA合成受损可能是由于疟疾感染引起的缺氧所致。