Organophosphate pesticides can interfere with the serotonergic nervous system and potentially lead to malformations and behavioral abnormalities during early development in sea urchin. To investigate the mechanism by which monocrotophos (MCP) pesticide disrupts the serotonergic nervous system, we evaluated its effects on serotonin metabolism. Fertilized embryos of sea urchin were incubated with 40% MCP pesticide at nominal concentrations of 0.01, 0.10 and 1.00mg/L, and the effects on tryptophan hydroxylase of Hemicentrotus pulcherrimus (HpTPH), serotonin reuptake transporter (SERT), monoamine oxidase (MAO), and serotonin levels were investigated. The results indicated that MCP pesticide disturbed the baseline pattern of HpTPH and SERT mRNA expression and MAO activity during early development in H. pulcherrimus. When serotonin should be quickly metabolized at 36-hpf stage, HpTPH and SERT expression was decreased and MAO activity was induced by MCP pesticide, leading to the impairment of serotonergic synaptic activity. But when serotonin should be metabolized at low levels during the other six stages, MCP pesticide induced HpTPH and SERT expression, resulting in the improvement of serotonergic synaptic activity. We concluded that this metabolic disturbance is one of the major mechanisms by which MCP pesticides affect the serotonergic nervous system and potentially contribute to various developmental abnormalities.
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