Hernandez J, Giralt M, Belloso E, Rebollo D V, Romero B, Hidalgo J
Departmento de Biologia Celular y Fisiologia, Falcultad de Ciencias, Universidad Autónoma de Barcelona, Spain.
Chem Biol Interact. 1996 Mar 8;100(1):27-40. doi: 10.1016/0009-2797(95)03683-0.
The interaction of Zn, stress and endotoxin on liver metallothionein (MT) regulation has been studied in the rat. Zn, stress and endotoxin increased liver MT levels significantly, by 12-, 5- and 8-fold, respectively. The previous administration of Zn to stress or endotoxin treatments increased MT levels by 35- and 42-fold, respectively, indicating a synergistic effect in both cases. In contrast, when liver MT was preinduced by stress, MT levels were further increased by endotoxin only in an additive manner. In another experiment where liver MT induction by stress was studied in control rats and in rats with preinduced MT by Zn, endotoxin or stress, it was found that Zn pretreated animals had higher MT-I mRNA levels than endotoxin- or stress-pretreated ones. No synergisms between dexamethasone, Zn, TNF and IFN were observed in primary culture of hepatocytes. These results suggest that the observed synergisms between Zn and other MT inducers in vivo in the liver is a consequence of increased Zn levels in the body and mobilization capacity, with concomitant MT synthesis.
在大鼠中研究了锌、应激和内毒素对肝脏金属硫蛋白（MT）调节的相互作用。锌、应激和内毒素分别使肝脏MT水平显著升高12倍、5倍和8倍。在应激或内毒素处理前给予锌，MT水平分别升高35倍和42倍，表明在这两种情况下均有协同作用。相反，当肝脏MT由应激预先诱导时，内毒素仅以相加的方式进一步提高MT水平。在另一项实验中，在对照大鼠以及经锌、内毒素或应激预先诱导MT的大鼠中研究应激对肝脏MT的诱导作用，发现锌预处理的动物比内毒素或应激预处理的动物具有更高的MT-I mRNA水平。在肝细胞原代培养中未观察到地塞米松、锌、肿瘤坏死因子（TNF）和干扰素（IFN）之间的协同作用。这些结果表明，在体内肝脏中观察到的锌与其他MT诱导剂之间的协同作用是体内锌水平升高和动员能力增强以及伴随MT合成的结果。
