CALCIUM HOMEOSTASIS AND EARLY EMBRYOTOXICITY IN MARINE-INVERTEBRATES

Chemicals of various origins: chlorambucil, maitotoxin, sigmoidines, c aulerpenyne, tributyltin, thapsigargin, 2,4,5-trichlorophenoxyacetic a cid (2,4,5-T) and retinoid CD 367 were assayed on the cleavage of sea urchin eggs, their embryonic development and mechanisms regulating Ca2 +. homeostasis. Compounds were used at therapeutic doses or at concent rations which were previously shown to be cytotoxic. These molecules d id not affect the fertilization of Paracentrorus lividus eggs but all of them delayed the first cleavage. Only chlorambucil and CD 367 retar ded hatching. All compounds provoked embryonic abnormalities if develo pment was followed up to the pluteus stage, 72 hr after fertilization. Chemicals inhibited the ability of ATP-driven Ca2+ accumulation by th e eggs in non-mitochondrial intracellular stores. Chlorambucil, maitot oxin and sigmoidines provoked a release of the Ca2+ sequestered with k inetics comparable to those provoked by the Ca2+ ionophore A23187. Ca2 + permeability of the plasma membrane was greatly increased by maitoto xin and 2,4,5-T whereas the other compounds were without effect. A dru g-induced change in the Ca2+ storage capacity of sea urchin eggs resul ting in retardation of cleaving stages and in further developmental de fects is discussed in view to the possibility of relating changes in C a2+-homeostasis with teratogenicity.