Sidransky H, Verney E
Department of Pathology, George Washington University Medical Center, Washington, DC 20037, USA.
Toxicology. 1997 Mar 14;118(1):37-47. doi: 10.1016/s0300-483x(96)03588-3.
This study describes that the affinity for specific L-tryptophan binding to hepatic nuclei in vitro is markedly decreased in NZBWF1 mice in comparison to that in Swiss mice. Also, the hepatic nuclei of NZBWF1 mice have a significantly decreased binding response in vitro to Showa Denko L-tryptophan (implicated in the eosinophilia-myalgia syndrome) or to its contaminants, 1,1'-ethylidenebis(tryptophan) or 3-phenylamino-L-alanine, when each is added to control, non-implicated L-tryptophan compared with hepatic nuclei of Swiss mice. Enhanced hepatic protein synthesis induced by tube-feeding control L-tryptophan is much less in NZBWF1 mice than in Swiss mice. Tube-feeding of Showa Denko L-tryptophan induced less stimulation of hepatic protein synthesis than did control L-tryptophan in Swiss mice but essentially none in NZBWF1 mice. NZBWF1 mice have a genetically altered response to L-tryptophan which may prove to be useful is studying the role of L-tryptophan in health and in disease.
本研究表明，与瑞士小鼠相比，NZBWF1小鼠体内特定L-色氨酸与肝细胞核的体外亲和力显著降低。此外，当将昭和电工L-色氨酸（与嗜酸性粒细胞增多性肌痛综合征有关）或其污染物1,1'-亚乙基双（色氨酸）或3-苯基氨基-L-丙氨酸分别添加到对照、无关的L-色氨酸中时，与瑞士小鼠的肝细胞核相比，NZBWF1小鼠的肝细胞核在体外对它们的结合反应明显降低。与瑞士小鼠相比，经管饲对照L-色氨酸诱导的NZBWF1小鼠肝脏蛋白质合成增强程度要小得多。在瑞士小鼠中，管饲昭和电工L-色氨酸诱导的肝脏蛋白质合成刺激作用比对照L-色氨酸小，但在NZBWF1小鼠中基本无刺激作用。NZBWF1小鼠对L-色氨酸有基因改变的反应，这可能在研究L-色氨酸在健康和疾病中的作用方面很有用。
