THE MURINE MUTATION, LETHAL MILK, RESULTS IN PRODUCTION OF ZINC-DEFICIENT MILK
THE MURINE MUTATION, LETHAL MILK, RESULTS IN PRODUCTION OF ZINC-DEFICIENT MILK
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DOI：
10.1093/jn/122.6.1214
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发表时间：
1992-06-01
影响因子：
4.2
通讯作者：
MERCER, JFB
中科院分区：
文献类型：
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作者：
ACKLAND, ML;MERCER, JFB
喂养具有致死性乳汁（lm）突变纯合子的母鼠的正常或突变幼崽会因缺锌而死亡。之前对突变乳中锌浓度的测定一直存在矛盾。这项工作表明，相对于喂养正常母鼠的正常和突变幼鼠，向哺乳母鼠腹腔注射 Zn-65 后，正常幼鼠和突变幼鼠喂养突变母鼠后，胃中的 Zn-65 量减少了 50-60%，肠道中减少了 25-30%，血液和胴体中恢复了 50-75%。对于喂养突变母鼠的幼鼠，通过原子吸收光谱法测定胃及其内容物的锌浓度，发现其为144 nmol/g湿重（对于突变幼鼠）和147 nmol/g湿重（对于正常幼鼠）。喂养正常母鼠的幼鼠胃锌浓度为 322 nmol/g 湿重（突变幼鼠）和 312 nmol/g 湿重（正常幼鼠）。给正常和突变成年小鼠口服 Zn-65 (27 kBq)，结果显示 24 小时后，Zn-65 在肝脏、肠道、肺、脾、肾、脑、皮肤、血液、胰腺或心脏或屠体中的分布没有显着差异。我们得出的结论是，致死性牛奶突变的主要影响是产生缺锌牛奶。
Normal or mutant pups that nurse dams homozygous for the lethal milk (lm) mutation die as a result of zinc deficiency. Previous determinations of the zinc concentration of the mutant milk have been conflicting. This work demonstrates that the amount of Zn-65 recovered in the organs of pups following an intraperitoneal injection of Zn-65 to lactating dams was reduced 50-60% in the stomach, 25-30% in the gut and 50-75% in the blood and carcass, for both normal and mutant pups nursing mutant dams, relative to pups nursing normal dams. For pups nursing mutant dams, the zinc concentration of the stomach and contents was determined by atomic absorption spectrometry and found to be 144 nmol/g wet wt (for mutant pups) and 147 nmol/g wet wt (for normal pups). Pups nursing normal dams had stomach zinc concentrations of 322 nmol/g wet wt (mutant pups) and 312 nmol/g wet wt (normal pups). Administration of an oral dose of Zn-65 (27 kBq) to normal and mutant adult mice showed that after 24 h there was no significant difference in the distribution of Zn-65 in the liver, gut, lung, spleen, kidney, brain, skin, blood, pancreas or heart or in the carcass. We conclude that the major effect of the lethal milk mutation is the production of Zn-deficient milk.