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Toxicokinetics makes up the background for predicting concentrations of chemicals in organisms and, thus, ecological risk assessment. However, physiological and toxicological mechanisms behind toxicokinetics of particular chemicals are purely understood. The commonly used one-compartment model has been challenged recently, showing that in the case of metals it does not describe the pattern observed in terrestrial invertebrates exposed to highly contaminated food. We hypothesised that the main mechanism shaping toxicokinetics of metals in invertebrates at high exposure concentrations in food is the cellular damage to the gut epithelial cells. Gut damage should result in decreased metal assimilation rate, while shedding the dead cells - in increased elimination rate. We performed a typical toxicokinetic experiment, feeding the ground beetles Pterostichus oblongopunctatus food contaminated with Cd, Ni or Zn at 40 mM kg -1 for 28 days, followed by a depuration period of 14 days on uncontaminated food. The male beetles were sampled throughout the experiment for body metal concentrations and histopathological examinations of the midgut. All metals exhibited a complex pattern of internal concentrations over time, with an initial rapid increase followed by a decrease and fluctuating concentrations during further metal exposure. Histopathological studies showed massive damage to the midgut epithelium, with marked differences between the metals. Cd appeared the most toxic and caused immediate midgut cell degeneration. The effects of Ni were more gradual and pronounced after at least 1 week of exposure. Zn also caused extensive degeneration in the gut epithelium but its effects were the weakest among the studied metals.

Metal toxicokinetics and metal-driven damage to the gut of the ground beetle Pterostichus oblongopunctatus