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    Environmental Modeling
     
    Physiologically Based Toxicokinetic Modeling of Mercury in Freshwater Fish
    As a trace element, mercury is present in all natural systems, and thus all organisms have some small amount of tolerance for this substance in minute doses. In larger concentrations, however, mercury can be quite harmful or even fatal. Throughout the world mercury has come under widespread use in industry, agriculture, and medicine, increasing the risk for people to become ill or die due to the ingestion of fish tainted with mercury. In recent years much work has been done to assess the effects of mercury on both fish and their predators, including humans.
    For this project, applied mathematicians at MathEcology developed a physiologically based toxicokinetic model to predict the uptake and distribution of methyl mercury in fish, with specific focus on species of freshwater fish commonly used for human consumption.
    Physiologically based toxicokinetic models for organic chemicals divide the fish into five tissue compartments: liver, kidney, fat, richly perfused (stomach, intestines, spleen, and gonads), and poorly perfused (white muscle, skin, and fins) tissue groups. The uptake and elimination of the chemical at the gills was modeled as countercurrent exchange processes, parametrized for trout.
    Methyl mercury has a very low octanol-water partition coefficient, which impedes its uptake by biological cells (though it can bind with organic matter in the water column before entering the fish’s system and thus be more readily absorbed and retained be tissues, and less readily excreted). There are several methods of movement of solutes across membranes, however here we were concerned with passive diffusion down the activity gradient, which can be described by Fick’s Law in combination with flow-limited uptake. In developing the system, we modeled the gill area as a function of body size, and thus included growth effects.
    At high initial concentrations of methyl mercury, the fish epithelium can become damaged or a mucous layer can form on the outside of the lamellae, effectively increasing the thickness of the epithelium and decreasing the flux of chemical across the gills. In extreme cases, this damage can be so severe that the gills fail entirely and the fish essentially "drowns". We modeled the uptake of methyl mercury by the fish as being governed by both passive diffusion and flow-limited uptake, in that the most restricted method of uptake became the limiting case.
    To model the rate of change of concentration of methyl mercury in the various compartments for the model, it is important to understand the partitioning of the chemical in the different biological phases of the organism. For partition coefficients less than one, the concentration in venous blood is greater than the concentration in the tissues in the compartment; for coefficients greater than one, the concentration in the tissues is greater than that in the venous blood. When the venous blood has a higher concentration of methyl mercury than does the arterial blood entering the compartment, the amount of toxicant in the compartment is decreasing and the tissues are eliminating the chemical. When the arterial blood has a higher concentration than the venous blood, bioaccumulation is occurring within the compartment.

    Extrabranchial elimination was quantified by first order and Michaelis-Menten elimination, which is limited by Vmax, the maximum chemical uptake rate.

    One of the assumptions of the model was a constant environmental concentration of methyl mercury, which was not represented per se by the experimental data. The equilibria predicted by the theoretical model indicated that long-term concentrations in kidney and muscle should be highest, followed by concentrations in the liver. The experimental data, however, exhibited higher long-term concentrations in the liver than in the muscle. This may have been due to several factors: the partition coefficients in the model neglected binding of mercury compounds to proteins in the tissues; extrabranchial elimination was not included in the equilibrium values calculated for both liver and kidneys; and chemical elimination and demethylation was neglected in the differential equations for all compartments.

     
     


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