Spermiotoxicity and embryotoxicity of triphenyltin (TPT) to the sea urchin Paracentrotus lividus Lmk

The most important sources of pollution by triphenyltin (TPT) in marine coastal ecosystems are its employment as a fungicide in agriculture and, in association with tributyltin, as a biocide in anti-fouling paints. In this study, spermiotoxicity and embryotoxicity (from post-fertilisation to pluteus stage) experiments were carried out to better clarify the ecotoxicological effects of TPT during the development of the sea urchin Paracentrotus lividus. Sperm exposed to triphenyltin acetate (TPTA) for 60 minutes showed a significantly reduced capability to fertilise eggs even at the lowest concentration of 0.1 µg TPTA l-1. In proportion to increasing concentrations, the percentage of fertilised eggs decreased, falling to 45% at 10 µg TPTA l-1, the maximum tested concentration. In embryotoxicity experiments at 48 h post-fertilisation, the length of the pluteus somatic rods was significantly reduced (P<0.001) from 1.5 µg l-1. Progressive increases in skeletal anomalies were also detected, highly significant (P <0.001) at 2 µg l-1. Embryonic development was greatly slowed at the highest TPT concentrations: embryos never reached the pluteus stage at 5 µg l-1, and development was blocked at the gastrula stage at 10 µg l-1. As observed in previous experiments using butyltin compounds, embryotoxic effects on both skeletal deposition and blocked development are presumed to be due to interference of TPT with intracellular calcium homeostasis. Sea urchin gametes are more sensitive to TPT than embryos, this condition emphasising the environmental risk due to TPT contamination.