Neurotoxicology 1997 Jan 01;183:841-50.

Methylmercury decreases IL-1beta immunoreactivity in the nervous system of the developing frog Xenopus laevis.

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In aquatic ecosystems, mercury can become methylated and act as a potent environmental toxin, producing developmental and neurotoxic effects in a variety of species, including frogs. Molecular indicators provide a means of assessing exposure to methylmercury and for understanding how it and other environmental toxins alter cellular function. Molecules such as growth or survival factors, and cytokines are good candidates for molecular indicators of exposure and/or damage because they are intimately related to cell and molecular processes that underlie normal growth and function. The cytokine, IL-1beta, was measured in whole frog embryos using Western blot methods and in specific structures using immunocytochemistry after exposure to 0, 10, 25, 50 and 100 parts per billion (ppb) methylmercury chloride (mmc). We observed no significant changes in total IL-1beta in whole embryo extracts. However, statistically significant decreases in IL-1beta were observed in the Vth cranial ganglion and myotomal blocks of Xenopus laevis embryos exposed to concentrations greater than or equal to 50 ppb mmc. In addition, increased mortality and alterations in gross morphology and behavior were altered by these same concentrations of mmc. Thus, frog embryos are highly susceptible to low levels of mmc contamination, and IL-1beta is an indicator of mmc exposure in the nervous system.

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