The heat-shock response in vivo: experimental induction during mammalian organogenesis.
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.
D000014:Abnormalities, Drug-Induced / Q000378:metabolism*; D000818:Animals; D001151:Arsenic / Q000633:toxicity*; D018053:Arsenites; D001402:B-Lymphocytes / Q000187:drug effects / Q000378:metabolism; D001853:Bone Marrow / Q000187:drug effects / Q000378:metabolism; D000013:Congenital Abnormalities / Q000209:etiology* / Q000378:metabolism; D004622:Embryo, Mammalian; D005314:Embryonic and Fetal Development; D005260:Female; D005333:Fetus; D006360:Heat-Shock Proteins / Q000096:biosynthesis*; D006358:Hot Temperature; D006801:Humans; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D011247:Pregnancy; D017670:Sodium Compounds
D018053:Arsenites; D006360:Heat-Shock Proteins; D017670:Sodium Compounds; C017947:sodium arsenite; D001151:Arsenic