The gastrointestinal tract is directly exposed to bisphenol A (BPA)-tainted foods and beverages stored in polycarbonate plastic containers. The effect of BPA on the movement of small intestine has not been reported until now. We report here the effect of BPA on the movement of the duodenum ex vivo in a rat model. We found significant inhibition of duodenal movement by BPA (10-320 µM). We suggest that BPA-induced inhibition of duodenal movement might be due to the suppression of stimulatory and/or activation of inhibitory motor neurons in enteric plexuses innervating the longitudinal and circular visceral smooth muscle cells in the duodenal wall. We observed a significant reversal of BPA-induced depression of duodenal movement by methylene blue, a soluble guanylyl cyclase blocker and N-ω-nitro-L-arginine methyl ester, a nitric oxide (NO) synthase inhibitor; but significant potentiation of the movement by sodium nitroprusside, a NO donor. From the results, we may suggest that BPA-induced inhibition of the movement might be partially due to activation of inhibitory motor neurons that secrete NO, a relaxant, on to smooth muscle cells. Furthermore, we found significant reversal of BPA-induced depression of the movement in phentolamine, an α-adrenergic receptor blocker, pretreated preparation. This result proves that norepinephrine secreting motor neurons may also be involved in BPA-induced inhibition of the movement. From the results, we conclude that BPA inhibits the movement of the duodenum through NO-mediated soluble guanylyl cyclase and α-adrenergic signaling pathways in visceral smooth muscle cells.

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The aim of the present study was to examine the effect of BPA (50mg/kgBW/day for 20 and 30 days exposure period) on the movement of duodenum in rat model. It was observed that BPA significantly depresses the amplitude and frequency of duodenal movements in test animals of both exposure groups. Besides, the activity of acetylcholinesterase (AChE) of duodenal tissue homogenate was also increased significantly in test animals. From the results it is suggested that BPA inhibits the movement of duodenum presumably by inducing the activity of AChE in smooth muscle membrane. We also found significant facilitation in nitric oxide synthase (NOS) expression and increase in deposition of calcium salts in Von Kossa's stained duodenal smooth muscle tissue section in test animals. From the results we may suggest that BPA may inhibit the duodenal movement by facilitating the synthesis of nitric oxide (NO) and decreasing the availability of free Ca 2+ in duodenal smooth muscle cells. In order to study the BPA induced oxidative stress in duodenal smooth muscle, we have measured the oxidative stress indices in duodenal tissue homogenate. We found that BPA significantly decreases the activity of antioxidant enzymes. Thus, we may conclude that BPA inhibits the motor function of duodenal smooth muscle presumably by inducing oxidative stress, decreasing the availability of free Ca 2+ , inducing the activity of AChE and promoting the synthesis of NO in duodenal smooth muscle cells.

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