Most of the methylmercury, when dissolved in corn oil, injected into the air cell passes through the inner shell membrane and into the egg albumen. Our final protocol used corn oil injections into the air cell, which are easier and safer than albumen injections. Although solvents can be injected directly into the albumen of an egg, high embryo mortality can occur in the solvent controls because of the formation of air bubbles in the albumen. Therefore, in the final protocol we standardized the time of injection to occur when each species reached the morphologic equivalent of a 3-day-old chicken embryo. The embryonic stage at which eggs were injected with corn oil altered mercury toxicity at early stages, the corn oil itself was toxic. Several solvents were tested, and corn oil at a rate of 1 :l/g egg contents was selected for the final standardized protocol because it had minimal toxicity to embryos and because methylmercury dissolved in corn oil yielded a dose?response curve in a range of egg concentrations that was similar to the range that causes reproductive impairment when the mother deposits methylmercury into her own eggs. A smaller amount of work was done with double-crested cormorant (Phalacrocorax auritus) eggs collected from the wild. Most of our experiments were done with chicken (Gallus domesticus), mallard (Anas platyrhynchos), and ring-necked pheasant (Phasianus colchicus) eggs, all of which were purchased in large numbers from game farms. During the course of developing this protocol, we investigated the effects of various factors on the toxicity of the injected methylmercury. We developed a standardized protocol for comparing the sensitivities of the embryos of different bird species to methylmercury when methylmercury was injected into their eggs. PRINCIPAL CONCLUSIONS: The lasting functional changes caused.įactors affecting the toxicity of methylmercury injected into eggs The functional deficits caused by prenatal methylmercury exposure appear to be permanent, and their extent may depend on the joint effect of toxicants and nutrients. of certain brain functions, thereby causing confounding bias. This notion is considered from epidemiological evidence using developmental methylmercury neurotoxicity as an example.
Essential nutrients may promote the development.PURPOSE: Adverse health effects of developmental toxicants may induce abnormal functional programming that leads to lasting functional deficits. Neurobehavioral outcomes are usually non-specific, and imprecise exposure assessment results in a bias toward the null. : Accumulating evidence indicates that adverse effects may occur even at low-level methylmercury exposures from seafood and freshwater fish. Methylmercury toxicity and functional programming The lasting functional changes caused by neurodevelopmental methylmercury toxicity fit into the pattern of functional programming, with effects opposite to those linked to beneficial stimuli. Essential nutrients may promote the development of certain brain functions, thereby causing confounding bias. Accumulating evidence indicates that adverse effects may occur even at low-level methylmercury exposures from seafood and freshwater fish. Methylmercury toxicity and functional programming.Īdverse health effects of developmental toxicants may induce abnormal functional programming that leads to lasting functional deficits.
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