Acute administration of tributyltin and trimethyltin modulate glutamate and N-methyl-D-aspartate receptor signaling pathway in Sebastiscus marmoratus.

Tributyltin (TBT), widely used as an antifouling biocide, is the most abundant pesticide in coastal environments. Trimethyltin (TMT) is a potent neurotoxicant of a mechanism of action yet to be uncovered. The neurotoxicity of TBT and TMT on the brain of marine fish Sebastiscus marmoratus was investigated in this study. The results showed that TBT and TMT can modulate amino acid neurotransmitters and N-methyl-D-aspartate receptor (NMDAR) signaling pathway in the brain of marine fish in a different manner. TBT did not increase the content of the amino acid neurotransmitters except gamma-aminobutyricd acid (GABA). TMT increased the content of aspartate (Asp), glutamate (Glu) and GABA in a dose-dependent manner. The expression of NADAR and components on its signaling pathway, such as calmodulin, calmodulin-dependent kinase II (CaMKII) and cAMP-response element-binding (CREB) protein was significantly decreased in a dose-dependent manner after TBT exposure. However, the low dose of TMT exposure up-regulate rather than down-regulate the expression of NMDAR and other genes of its pathway. It is suggested that the Glu-NMDAR pathway plays a role in the mechanism for the brain injury in marine fish after TBT or TMT exposure. The alteration of expression of glutamatergic receptor NMDAR and components on its signaling pathway accompanied with the change of total brain transmitter level indicated the importance of glutamatergic system in organotin toxicity.