Abstract
The current studies were undertaken to examine the effects of the various prostaglandins (PG) on zinc transport across the rat small intestine. In in vitro studies using everted jejunal sacs, the addition of PGE2 to the mucosal media increased the transport of 65Zn from the mucosal surface to the serosal surface by 54%, whereas the addition of PGF2 decreased it by 40%. In contrast, addition of PGE2 to the serosal media decreased 65Zn transport from serosa to mucosa by 37% while the addition of PGF2 increased it by 36%. Our in vivo studies showed that oral administration of PGE2 caused a 2-fold increase in the 65Zn content of rat internal organs whereas PGF2 decreased it slightly but insignificantly. Pretreatment of rats with indomethacin resulted in a significant decrease in organ 65Zn content when compared to control, when the rats were administered 65Zn content when compared to control, when the rats were administered 65Zn by the oral route. The decrease in organ 65Zn content was overcome by the administration of PGE2. Furthermore, the administration of PGF2 to indomethacin pretreated rats caused a further and significant decrease in the 65Zn content of liver and pancreas—the two organs that have a high zinc uptake. The fact that PG had no effect on the active transport of L-[3-3H]histidine and that PGE2 and PGF2 had opposing effects on zinc transport strongly suggest that PGE2 and PGF2 act as physiological regulators of zinc transport by the intestinal mucosa, and that their effects are specific.