Microcystin-LR promote intestinal secretion of water and electrolytes in rats

Abstract

We showed previously that exposure to microcystin-LR causes renal toxic effects in isolated perfused rat kidney, and that inflammatory mediators from supernatants of macrophages stimulated by microcystin-LR are involved in this process. The aim of this research was to examine water and electrolytes secretion in vivo, induced by microcystin-LR and supernatant of macrophages stimulated for this toxin (SUP.MϕS+MCLR), using perfused rat ileal segment and ligated intestinal loop models. We found microcystin-LR at 1 μg/ml (0.09±0.003* vs. control 0.07±0.001 g of secretion/2 cm of loop; P<0.05*) and the SUP.MϕS+MCLR after 18 h postinoculation (0.10±0.003 vs. control 0.03±0.002 g/cm) caused intestinal secretion. In addition, microcystin-LR caused significant sodium secretion (−2.18±0.72* vs. control 2.18±0.50 μEq g −1 min −1), potassium (−0.26±0.04* vs. control 0.32±0.03 μEq g −1 min −1), chloride (MCLR=−3.29±1.93* vs. control 0.88±1.25 μEq g −1 min −1) and water (−0.012±0.004* vs. control 0.002±0.002 ml g −1 min −1). We also demonstrated SUP.MϕS+MCLR to induce intestinal secretion of electrolytes (sodium, potassium, chloride) and water. These findings suggested that microcystin-LR and lamina propria macrophages-derived mediators are able to induce intestinal secretion in vivo, probably via inhibition of protein phosphatase.