Mastrogiacomo F, LaMarche J, Dozić S, Lindsay G, Bettendorff L, Robitaille Y, Schut L, Kish S J
Human Neurochemical Pathology Laboratory, Clarke Institute of Psychiatry, Toronto, Canada.
Neurodegeneration. 1996 Mar;5(1):27-33. doi: 10.1006/neur.1996.0004.
Enzyme activities of a alpha-ketoglutarate dehydrogenase complex (alpha KGDHC) and one of its constituent subunits, dihydrolipoamide dehydrogenase (E3), are reported to be reduced in non-CNS tissues of some patients with Friedreich's ataxia (FA); however, the results are highly conflicting. To determine whether an enzyme abnormality occurs in brain, we measured immunoreactive levels of the three alpha KGDHC subunits, namely, alpha-ketoglutarate dehydrogenase (E1), dihydrolipoamide succinyltransferase (E2) and E3 in postmortem frontal, occipital and cerebellar cortices of 18 control subjects, 9 patients with FA and, for comparison, 12 patients with spinocerebellar ataxia type 1 (SCA1). Decreased (-20 to -31%) levels of E3 were observed in all three examined areas of the patients with FA with the changes statistically significant in cerebellar and frontal cortices. The E3 reduction could be explained by a loss of alpha KGDHC or other dehydrogenase complexes (e.g. pyruvate dehydrogenase complex) which utilize this subunit. In SCA1, enzyme changes were limited to E2 in cerebellar (-26%) and frontal (-19%) cortices. Although the E3 and E2 reductions are only slight, and may represent secondary events, the changes in this key Krebs cycle enzyme could exacerbate degenerative processes in both of the spinocerebellar ataxia disorders.
据报道,在一些弗里德赖希共济失调(FA)患者的非中枢神经系统组织中,α-酮戊二酸脱氢酶复合体(αKGDHC)及其组成亚基之一二氢硫辛酰胺脱氢酶(E3)的酶活性降低;然而,结果存在高度冲突。为了确定大脑中是否发生酶异常,我们测量了18名对照受试者、9名FA患者以及作为对照的12名1型脊髓小脑共济失调(SCA1)患者死后额叶、枕叶和小脑皮质中αKGDHC的三个亚基,即α-酮戊二酸脱氢酶(E1)、二氢硫辛酰胺琥珀酰转移酶(E2)和E3的免疫反应水平。在FA患者的所有三个检查区域均观察到E3水平降低(-20%至-31%),在小脑和额叶皮质中变化具有统计学意义。E3的降低可能是由于αKGDHC或其他利用该亚基的脱氢酶复合体(如丙酮酸脱氢酶复合体)的丧失。在SCA1中,酶变化仅限于小脑(-26%)和额叶(-19%)皮质中的E2。尽管E3和E2的降低幅度较小,可能代表继发事件,但这种关键的三羧酸循环酶的变化可能会加剧这两种脊髓小脑共济失调疾病的退行性过程。