Combined Exposure to Ecologically Relevant Concentrations of Atrazine and Microcystin Causes Morphological Changes in the Hepatopancreas of Crayfish.

Aquatic environments are contaminated through anthropogenic activities, leading to an increase in a variety of pollutants, including pesticides and algal toxins. The cyanobacterium Microcystis aeruginosa produces the toxin microcystin with leucine and arginine (MC-LR) and is found in various freshwater environments. MC-LR causes liver and tissue damage in aquatic organisms. Atrazine is a commonly applied herbicide in the United States and is toxic following acute exposures. These toxins can often be found together in aquatic environments and thus may lead to combined toxicological effects; however, very little information is available regarding their cumulative effects on tissues such as the hepatopancreas (or liver). To examine the combined effects, we exposed crayfish (Faxonius virilis) to 10 ppb atrazine, 10 ppb MC-LR, a combination of 10 ppb of both, and a control for 96 hours. The hepatopancreas was examined and tubular morphology of each group of crayfish was compared. We found that morphological defects such as vacuolization, lumen dilation, and epithelial degeneration were seen following exposures to both atrazine and MC-LR individually and in combination. Combined exposures led to a significant increase in vacuolization of tubular epithelium. Following all exposures, lumen proportion increased, epithelial height decreased, and there was degeneration of the microvillar brush border. Overall, hepatopancreas morphology was significantly altered post-exposure in all treatments. These changes could lead to impairment of hepatopancreas and subsequent changes in biotransformation, detoxification, digestion, reproduction, and molting, causing a reduction in crayfish population size. Furthermore, similar cellular and morphological changes may also occur in other crustaceans inhabiting the same environment.