Dave Bharat N, Katyare Surendra S, Billimoria Framroze R
Department of Biochemistry, Seth G.S. Medical College and K.E.M. Hospital, Parel, Mumbai 400012, India.
Neurosci Lett. 2006 Feb 27;395(1):33-6. doi: 10.1016/j.neulet.2005.10.049. Epub 2005 Nov 15.
Effect of neonatal hypothyroidism on kinetic properties of Ca(2+)-ATPase from rat brain synaptic plasma membranes and microsomes were examined. Neonatal hypothyroidism resulted in significant decrease in the enzyme activity in both the membrane systems. The synaptic membranes in control group displayed presence of one kinetic component whereas a low affinity component became evident in the hypothyroid group. In the microsomes, both control as well as hypothyroid groups showed presence of two kinetic components with the latter group showing two-fold increase in the K(m). The Ca(2+) binding characteristics were generally unaltered in the enzyme from both the membrane systems. Our results suggest that impairment in the Ca(2+)-ATPase activity together with altered kinetic properties could be one of the underlying biochemical mechanisms leading to CNS dysfunction as a consequence of thyroid hormone deprivation during critical stages of brain development.
研究了新生儿甲状腺功能减退对大鼠脑突触质膜和微粒体中Ca(2+)-ATP酶动力学特性的影响。新生儿甲状腺功能减退导致两个膜系统中的酶活性显著降低。对照组的突触膜表现出一种动力学成分,而甲状腺功能减退组中低亲和力成分变得明显。在微粒体中,对照组和甲状腺功能减退组均表现出两种动力学成分,后者的K(m)增加了两倍。两个膜系统的酶中Ca(2+)结合特性通常未改变。我们的结果表明,Ca(2+)-ATP酶活性受损以及动力学特性改变可能是脑发育关键阶段甲状腺激素缺乏导致中枢神经系统功能障碍的潜在生化机制之一。