Embryotoxic potency of 2,4,5-trichlorophenoxyacetic acid on sea urchin eggs: Association with calcium homoeostasis

The effect of 2,4,5-trichlorophenoxyacetic acid (2,4,5-T), a polychlorinated herbicide, on the early development of sea urchin eggs and on Ca(2+) permeability was investigated. Concentrations lower than 5 x 10(-4)m delayed the first cleavages and produced a teratogenic effect characterized by a large spectrum of structural malformations at the pluteus stage. The cleaving stage (pre-hatching) was the period most sensitive to the compound. Upper concentrations caused a stepwise dose-dependent lethality associated with arrest of cleavage. 2,4,5-T increased plasmalemma Ca(2+) permeability of unfertilized eggs by opening voltage-dependent Ca(2+) channels; verapamil (10(-4)m) and nifedipine (10(-4)m) abolished this effect. Ca(2+) permeability was also increased by 2,4,5-T after fertilization of the eggs. ATP-dependent intracellular sequestration of Ca(2+), measured in isolated cortices, was inhibited by 2,4,5-T. Ca(2+) movement was affected over a range of concentrations similar to those producing embryonic abnormalities and lethality. The results suggest that the teratogenic potency of 2,4,5-T is associated with delay in first cleavages and alterations in Ca(2+) homoeostasis.