作者: F.A.C. Wiegant , J.E.M. Souren , J. van Rijn , R. van Wijk
DOI: 10.1016/0300-483X(94)90034-5
关键词: Shock (circulatory) 、 Mechanism of action 、 Biology 、 Dinitrophenol 、 HSP60 、 Cell biology 、 Sodium arsenite 、 Heat shock protein 、 Programmed cell death 、 Cell physiology 、 Biochemistry
摘要: In order to determine whether induction of specific stress proteins is dependent on a given stressor and these linked survival, Reuber H35 rat hepatoma cells were exposed five different environmental stressors (heat shock, arsenite, cadmium, dinitrophenol ethanol). The effect was studied cell survival as well inhibition recovery protein synthesis heat shock (hsps). this article, we present evidence that several well-known hsp-inducers fail stimulate hsps in degree comparable the by shock. Most evidently, hsp60 not induced cadmium-treatment, whereas hsp100 hardly sodium arsenite. Treatment with DNP only slightly induces hsp68 hsp84, no detectable observed after treatment ethanol. contrast, cadmium raises amount hsp28 higher level compared A comparison stressor-specific major also made under conditions similar impact cellular physiology: (a) up critical point death starts occur, (b) iso-survival (50%). We conclude cannot be simply used general risk-assessment tool, validation warrants further research larger groups proteins.