CONICET | Buscador de Institutos y Recursos Humanos

ABSTRACT Anatoxin-a acts as a neuro-muscular blocking agent. Acute toxicity is characterized by rapid onset of paralysis, tremors, convulsions, and death. Human exposures may occur from recreational water activities and dietary supplements, but are primarily through drinking water. The current studies were conducted to: examine the effect of in utero exposure on postnatal viability, growth and neurodevelopment; evaluate in vitro embryotoxicity; and explore potential synergism with another algal toxin, microcystin-LR. Preliminary results on amphibian toxicity are reported. Time-pregnant mice received 125 or 200 µg/kg by intraperitoneal injection on gestation days (GD) 8-12 or 13-17. In both treatment periods maternal toxicity was observed at 200 µg/kg, but there were no significant treatment-related effects on pup viability or weight on postnatal day (PND) 1 or 6. GD 13-17 pups were evaluated on PND 6,12, and 20 for standard markers of neurodevelopmental maturation. No significant postnatal neurotoxicity was observed. GD 8 mouse embryos, exposed in vitro to 0.1 - 25µM for 26-28 h., exhibited perturbations in yolk sac vasculature in the absence of significant embryonic dysmorphology. Stages 17 and 25 toad embryos (Bufo arenarum), exposed to 0.03 - 30.0 mg/L for ten days, exhibited a transient narcosis. At the high dose in both groups 100% mortality occurred 6-13 days post-exposure, an uncharacteristic delay in toxicity. No deaths or definitive signs of intoxication were observed in mice receiving by gavage either 0, 500, or 1000µg/kg microcystin-LR and, ~ 50 minutes later, either 0, 500, 1000, or 2500µg/kg anatoxin-a. These studies indicate a lack of significant in vivo and in vitro developmental toxicity in the mouse, while early amphibian results suggest a delayed lethality. No synergism with microcystin-LR was noted by the oral route.

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