ABSTRACT
Triclosan (TCS, 2,4,4'-trichloro-2'-hydroxydiphenyl ether), a broad-spectrum antibacterial agent, is commonly found in the aquatic environment. In this study, we investigated TCS toxicity with pertaining to gamete viability, fertilization, and embryogenesis up to pluteus stage of the sea urchin, (Strongylocentrotus nudus). When the sperm and eggs were exposed to TCS (0-3.0 µM), the viability of sperm was significantly decreased at molarities higher than 1 µM of TCS. In addition, for exposure of 2.0 µM TCS the viability of eggs was not influenced and none of the sperm was viable. Fertilization rate was significantly decreased when sperm were exposed to 0.5 and 1 µM of TCS (p<0.001) and no fertilization was observed for the exposure of 1.5 µM of TCS. In embryonic development, embryos are treated with higher than 1.0 µM levels of TCS displayed arrested development. For TCS, the EC50 and LOECs values were 1.8, 1.49 and 0.99 µM and 0.53, 0.62 and 0.39 µM for sperm viability, fertilization rate, and larval development to pluteus, respectively. In the recovery test regarding normal development of arrested embryos based upon TCS exposure time, it was observed that embryos exposed to 1 µM TCS for 15 h were normally recovered for normal development, while embryos with more than 30 h exposure were not recovered to normal larvae. Overall, the results of this study strongly suggest that the gametes and embryos of S. nudus can provide the basis for an effective bioassay, with a fast and sensitive means of evaluating TCS contamination in the marine ecosystem.
Subject(s)
Sea Urchins/drug effects , Triclosan/toxicity , Water Pollutants, Chemical/toxicity , Animals , Embryo, Nonmammalian/drug effects , Embryonic Development/drug effects , Female , Fertilization/drug effects , Larva/drug effects , Male , Reproduction/drug effects , Spermatozoa/drug effectsABSTRACT
Go, a heterotrimeric G-protein, is enriched in brain and neuronal growth cones. Although several reports suggest that Go may be involved in modulation of neuronal differentiation, the precise role of Go is not clear. To investigate the function of Go in neuronal differentiation, we determined the effect of Goalpha, the alpha subunit of Go, on the expression of Ca(v)2.2, the pore-forming unit of N-type calcium channels, at the transcription level. Treatment with cyclic AMP (cAMP), which triggers neurite outgrowth in neuroblastoma F11 cells, increased the mRNA level and the promoter activity of the Ca(v)2.2 gene. Overexpression of Goalpha inhibited neurite extension in F11 cells and simultaneously repressed the stimulatory effect of cAMP on the Ca(v)2.2 gene expression to the basal level. Targeted mutation of the Goalpha gene also increased the level of Ca(v)2.2 in the brain. These results suggest that Go may regulate neuronal differentiation through modulation of gene expression of target genes such as N-type calcium channels.