BREAST-MILK JAUNDICE - INVITRO INHIBITION OF RAT-LIVER BILIRUBIN-URIDINE DIPHOSPHATE GLUCURONYLTRANSFERASE ACTIVITY AND Z-PROTEIN-BROMOSULFOPHTHALEIN BINDING BY HUMAN BREAST-MILK
BREAST-MILK JAUNDICE - INVITRO INHIBITION OF RAT-LIVER BILIRUBIN-URIDINE DIPHOSPHATE GLUCURONYLTRANSFERASE ACTIVITY AND Z-PROTEIN-BROMOSULFOPHTHALEIN BINDING BY HUMAN BREAST-MILK
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DOI：
10.1203/00006450-197606000-00007
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发表时间：
1976-01-01
影响因子：
3.6
通讯作者：
ODIEVRE, M
中科院分区：
文献类型：
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作者：
FOLIOT, A;PLOUSSARD, JP;ODIEVRE, M
对9例母乳性黄疸患儿母亲的24份母乳样品进行了研究。八个样本的牛奶从母亲的非黄疸婴儿，沿着与5个配方奶富含多不饱和脂肪酸，作为对照。母乳与黄疸的婴儿没有抑制作用时，立即解冻后进行测定。将这些奶样品在4 ℃下储存后，它们强烈抑制胆红素结合（尿苷二磷酸葡萄糖醛酸转移酶（UDPGT）活性的80.3%抑制）和溴磺酞（BSP）与细胞质Z蛋白的结合（染料结合抑制82.1%）。对BSP与Y蛋白的结合无影响。把牛奶加热到56度。以如下方式修改结果。当牛奶解冻后立即加热时，即使在储存96 h后也没有观察到抑制作用。当牛奶先贮存96 h后再加热时，其抑制作用与不加热贮存的牛奶相同。病理性母乳仅在储存条件下才会明显抑制BSP-Z蛋白结合，该条件也会导致出现体外抑制胆红素结合的能力，以及导致非酯化脂肪酸的释放。这种体外抑制能力的出现似乎与病理性乳汁特有的脂解活性有关。
Twenty-four samples of breast milk from 9 mothers of infants suffering from breast milk jaundice were studied. Eight samples of milk from mothers of nonjaundiced infants, along with 5 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. After these milk samples were stored at 4.degree., 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. Heating the milk to 56.degree. 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 h. When the milk was 1st stored at 96 h and then heated, it had the same inhibitory effects as the milks which were stored without heating. Pathologic breast milk will apparently 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 nonesterified fatty acids. The appearance of this inhibitory capacity in vitro seems linked to the lipolytic activity particular to pathologic milks.