Bienzle U, Effiong C E, Aimaku V E, Luzzatto L
Acta Haematol. 1976;55(1):10-20. doi: 10.1159/000207988.
Glucose-6-phosphate dehydrogenase (G6PD) deficiency is a major cause of severe neonatal jaundice in Nigeria, but not all G6PD-deficient babies become jaundiced. Neonatal jaundice not attributable to G6PD deficiency nor to any other known aetiology is also common. In an effort to explain these two facts, we have measured the levels of the three enzymes G6PD, glutathione peroxidase (GSHPX), and glutathione reductase (GSSGR) in 38 jaundiced newborns, 26 control newborns, and 44 normal adults, all of them males. We could not yet prove an additive effect of GSSGR or GSHPX deficiency with G6PD deficiency in causing jaundice. There was no evidence that low levels of GSHPX per se are associated with jaundice. However, jaundiced newborns with normal G6PD had significantly lower levels of GSSGR than control newborns with normal G6PD. These data suggest that a relatively low activity of GSSGR, a riboflavin-dependent enzyme, may predispose the red cells to accelerated destruction in the neonatal period.
葡萄糖-6-磷酸脱氢酶（G6PD）缺乏是尼日利亚新生儿严重黄疸的主要原因，但并非所有G6PD缺乏的婴儿都会出现黄疸。并非由G6PD缺乏或任何其他已知病因引起的新生儿黄疸也很常见。为了解释这两个事实，我们测量了38名黄疸新生儿、26名对照新生儿和44名正常成年人（均为男性）体内三种酶——G6PD、谷胱甘肽过氧化物酶（GSHPX）和谷胱甘肽还原酶（GSSGR）的水平。我们尚未证明GSSGR或GSHPX缺乏与G6PD缺乏在导致黄疸方面存在累加效应。没有证据表明GSHPX本身水平低与黄疸有关。然而，G6PD正常的黄疸新生儿的GSSGR水平明显低于G6PD正常的对照新生儿。这些数据表明，作为一种依赖核黄素的酶，GSSGR活性相对较低可能会使红细胞在新生儿期更容易加速破坏。
