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首页> 外文期刊>Pediatric Research >Breast Milk Jaundice: In Vitro Inhibition of Rat Liver Bilirubin-Uridine Diphosphate Glucuronyltransferase Activity and Z Protein-Bromosulfophthalein Binding by Human Breast Milk
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Breast Milk Jaundice: In Vitro Inhibition of Rat Liver Bilirubin-Uridine Diphosphate Glucuronyltransferase Activity and Z Protein-Bromosulfophthalein Binding by Human Breast Milk

机译:母乳性黄疸:体外抑制人乳汁对大鼠肝脏胆红素-尿苷二磷酸葡萄糖醛酸转移酶活性和Z蛋白-溴磺酞的结合。

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Extract: Twenty-four samples of breast milk from nine mothers of infants suffering from breast milk jaundice were studied. Eight samples of milk from mothers of nonjaundiced infants, along with five formula milks enriched with polyunsaturated fatty acids, served as controls. Milks from mothers with jaundiced infants had no inhibitory effect when assayed immediately after thawing. However, after these milk samples were stored at 4°, they strongly inhibited bilirubin conjugation (80.3% inhibition of uridine diphosphate glucuronyltransferase (UDPGT) activity) and bromosulfophthalein (BSP) binding to cytoplasmic Z protein (dye binding inhibited 82.1%). There was no effect on BSP binding to Y protein (see Table 1). Heating the milk to 56° modified the results in the following manner; when the milk was heated immediately after thawing, no inhibitory effect was seen, even after storage for 96 hr. On the other hand, when the milk was first stored at 96 hr and then heated, it had the same inhibitory effects as the milks which were stored without heating. The present study shows that pathologic breast milk will inhibit BSP-Z protein binding only when stored under conditions that also cause the appearance of the capacity to inhibit bilirubin conjugation in vitro, as well as causing the liberation of nonesterifled fatty acids. Thus, the appearance of this inhibitory capacity in vitro seems linked to the lipolytic activity particular to pathologic milks.Speculation: By demonstrating that the in vitro inhibition of bilirubin conjugation by pathologic milks is due to the tying up of hepatic transport proteins, we have furnished the missing link in the sequence of events following ingestion of potentially inhibitory milk resulting in neonatal jaundice. We call the pediatrician's attention to the key role of ingested free fatty acids in the etiology of this condition.
机译:提取物:研究了来自9名母亲患母乳性黄疸婴儿的24个母乳样品。八份来自非黄疸婴儿母亲的牛奶样品,以及五份富含多不饱和脂肪酸的配方奶粉作为对照。当解冻后立即进行分析时,母亲和黄疸婴儿的牛奶没有抑制作用。但是,在将这些牛奶样品保存在4°后,它们会强烈抑制胆红素结合(抑制尿苷二磷酸葡糖醛酸转移酶(UDPGT)活性的80.3%)和溴代磺酞(BSP)与细胞质Z蛋白的结合(染料结合抑制了82.1%)。对BSP与Y蛋白的结合没有影响(见表1)。将牛奶加热到56°可以通过以下方式改变结果:当融化后立即加热牛奶时,即使储存96小时也没有抑制作用。另一方面,当牛奶首先在96小时储存然后加热时,其抑制作用与未加热的牛奶相同。本研究表明,病理性母乳仅在储存于一定条件下才能抑制BSP-Z蛋白结合,这种条件还可能导致体外显示出抑制胆红素结合的能力,并导致非酯化脂肪酸的释放。因此,这种抑制能力的出现似乎与病理性乳汁特有的脂解活性有关。推测:通过证明病理性乳汁对胆红素的体外抑制作用是由于肝转运蛋白的结合,我们提供了摄入潜在的抑制性牛奶导致新生儿黄疸后,事件序列中的缺失环节。我们呼吁儿科医生注意摄入游离脂肪酸在此病因中的关键作用。

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