German J, Louie E, Banerjee D
Teratog Carcinog Mutagen. 1986;6(6):555-62. doi: 10.1002/tcm.1770060609.
According to the embryonic stress hypothesis of teratogenesis, anatomical malformation can be the consequence of the induction of a heat-shock response (HSR) in the embryo at some critical stage during the determination or differentiation of organs. This hypothesis states that a teratogen is any agent that is capable of inducing a HSR and that can reach the developing embryo. As a first step in determining whether the hypothesis is tenable, it was necessary to determine whether the embryo in fact is capable of making the HSR during the period of organogenesis. Pregnant mice were treated with two classical inducers of the HSR, one a physical and the other a chemical agent--namely, hyperthermia and sodium arsenite. The embryos, while still in the living mouse, responded with heat-shock protein induction, as did control bone marrow.
根据致畸作用的胚胎应激假说，解剖学上的畸形可能是在器官形成的某些关键阶段，胚胎中诱导产生热休克反应（HSR）的结果。该假说指出，致畸物是任何能够诱导热休克反应且能到达发育中胚胎的物质。作为确定该假说是否成立的第一步，有必要确定胚胎在器官发生期是否实际上能够产生热休克反应。用两种经典的热休克反应诱导剂——一种是物理剂，另一种是化学剂，即高温和亚砷酸钠处理怀孕小鼠。胚胎仍在活体内时，就像对照骨髓一样，通过诱导热休克蛋白作出反应。
