Apoptosis is an adaptive response in bovine preimplantation embryos that facilitates survival after heat shock.
Heat shock compromises development of preimplantation bovine embryos and the percentage of blastomeres labeled as TUNEL-positive. It was hypothesized that TUNEL labeling represents apoptosis and that apoptosis after heat shock is beneficial for continued embryonic development. To test these hypotheses, experiments were performed with z-DEVD-fmk, an inhibitor of group II caspases, on heat shock responses of embryos > or =16-cell stage at day 4 after insemination. Heat shock of 41 degrees C for 9 h increased group II caspase activity and the proportion of TUNEL positive cells; z-DEVD-fmk blocked these effects. The reduction in development of embryos exposed to heat shock for 6-9 h was magnified in the presence of z-DEVD-fmk. Results indicate that group II caspases mediate heat-induced apoptosis in bovine embryos and that inhibition of these caspases has a detrimental effect on embryonic resistance to heat shock. Apoptosis can be viewed as an adaptative mechanism to allow embryonic survival and development following stress.
Paula-Lopes
F F
FF
Department of Animal Sciences, University of Florida, P.O. Box 110910, Gainesville, FL 32611-0910, USA.
Hansen
P J
PJ
D000222:Adaptation, Physiological; D000818:Animals; D017209:Apoptosis; D001755:Blastocyst / Q000166:cytology* / Q000187:drug effects / Q000502:physiology; D001757:Blastomeres / Q000648:ultrastructure; D020169:Caspases / Q000378:metabolism; D002417:Cattle / Q000196:embryology* / Q000502:physiology; D002452:Cell Count; D015853:Cysteine Proteinase Inhibitors / Q000494:pharmacology; D005314:Embryonic and Fetal Development; D018869:Heat-Shock Response; D020287:In Situ Nick-End Labeling; D009842:Oligopeptides / Q000494:pharmacology
D015853:Cysteine Proteinase Inhibitors; D009842:Oligopeptides; C110772:benzoylcarbonyl-aspartyl-glutamyl-valyl-aspartyl-fluoromethyl ketone; D020169:Caspases