Host zinc metabolism and the Ehrlich ascites tumour. Zinc redistribution during tumour-related stress.

Host zinc metabolism and the Ehrlich ascites tumour. Zinc redistribution during tumour-related stress.
复制标题

宿主锌代谢和艾利希腹水瘤。

DOI:
10.1042/bj2330099
复制
发表时间:
1986
期刊:
The Biochemical journal
影响因子:
--
通讯作者:
Petering,DH
Petering,DH
中科院分区:
--
文献类型:
--
作者:
Ujjani,B;Krakower,G;Bachowski,G;Krezoski,S;Shaw3rd,CF;Petering,DH

文献摘要

相似文献

在注射艾氏腹水瘤细胞的小鼠中,研究了锌在血浆和肝脏之间的再分布。在24小时内注射血浆锌水平下降,锌出现在新合成的肝脏金属硫蛋白。这种反应取决于注射到宿主体内的肿瘤细胞的数量。锌的摄取进入肝脏,并在锌结合蛋白(被鉴定为金属硫蛋白)中特异性积累,持续数天,并在肿瘤生长停止时达到平台期。在此期间,血浆铜升高。这种再分配也发生在小鼠预处理镉在其饮用水1个月的水平为20,50和100微克/毫升。然而,在每种情况下,有一个滞后3天之前,锌增加这些动物的肝脏中已经含有大量的镉/锌-金属硫蛋白。当将埃利希细胞注射到先前被置于缺锌饮食数天的小鼠中时,血浆锌已经很低,并且没有锌净摄取到肝脏金属硫蛋白中是明显的。最后,它表明,腹水本身可以刺激宿主锌进入肝脏的瞬时转移。热灭活流体失去了这种性质。有人建议,在腹膜中,肿瘤细胞启动由腹水因子介导的应激反应。
Zinc redistribution between plasma and liver has been examined in mice injected with Ehrlich-ascites-tumour cells. Within 24 h of injection plasma Zn levels decrease and Zn appears in newly synthesized liver metallothionein. This response is dependent upon the number of tumour cells injected into the host. Uptake of Zn into liver and its specific accumulation in a Zn-binding protein, identified as metallothionein, continues for a number of days and reaches a plateau as tumour growth ceases. Over this time period, plasma copper rises. This redistribution also occurs in mice pretreated with cadmium in their drinking water for 1 month at levels of 20, 50, and 100 micrograms/ml. However, in each case there is a lag of 3 days before Zn increases in the livers of these animals which already contain substantial amounts of Cd/Zn-metallothionein. When Ehrlich cells are injected into mice previously placed on a Zn-deficient diet for several days, plasma Zn is already low and no net uptake of Zn into liver metallothionein is apparent. Finally, it is shown that ascites fluid can itself stimulate a transient shift of host of Zn into liver. Heat-inactivated fluid loses this property. It is suggested that, in the peritoneum, tumour cells initiate a stress response mediated by an ascites-fluid factor.