Embryonic and maternal heat shock responses to a teratogenic hyperthermic insult.
Exposing embryos to elevated temperatures both in vivo and in vitro has been shown to result in the production of offspring with severe congenital abnormalities. While a direct effect of heat cannot be excluded, recent interest has been focused on the possible role that the induction of the heat shock response may have in the etiology of the observed congenital defects. In the present study, mouse embryos from inbred strains known to differ in terms of their sensitivity to heat-induced exencephaly were treated in vivo and their heat shock response determined using SDS-PAGE electrophoretic techniques. Further, the embryonic responses were compared with a maternal cell type. We observed excellent agreement between the two test systems following exposure to a teratogenic hyperthermic insult. Both the embryonic and maternal cells underwent a reduction in total protein synthesis and an enhanced synthesis of four heat shock proteins migrating with the molecular weights of 68, 70, 97, and 110 kDa. The results failed to indicate any strong correlation between the heat shock response and enhanced genetic sensitivity to hyperthermia-induced neural tube defects.
Bennett
G D
GD
Department of Veterinary and Comparative Anatomy, Pharmacology and Physiology, Washington State University, Pullman 99164-6520.
Mohl
V K
VK
Finnell
R H
RH
D000818:Animals; D001831:Body Temperature / Q000187:drug effects; D000013:Congenital Abnormalities / Q000209:etiology / Q000503:physiopathology*; D004591:Electrophoresis, Polyacrylamide Gel; D004622:Embryo, Mammalian / Q000502:physiology*; D005260:Female; D006358:Hot Temperature / Q000009:adverse effects*; D008214:Lymphocytes / Q000502:physiology; D051379:Mice; D008811:Mice, Inbred DBA; D008815:Mice, Inbred Strains; D011247:Pregnancy; D013045:Species Specificity; D013312:Stress, Physiological / Q000503:physiopathology*