Ota S, Razandi M, Terano A, Hiraishi H, Ivey K J
Gastroenterol Jpn. 1987 Jun;22(3):285-91. doi: 10.1007/BF02774254.
Arachidonic acid is cytoprotective against ethanol damage in vivo. Stimulation of production of endogenous prostaglandin has been postulated as a mechanism of this protection. The current study assessed the ability of arachidonic acid to protect gastric mucosal cells directly and the effect of arachidonic acid on prostaglandin production. To determine cytoprotection, sodium taurocholate was used as a damaging agent and cell viability was assayed by 51Cr release in vitro. By the dose response curve, 5 mM sodium taurocholate was chosen for the protective study. Cells were preincubated with arachidonic acid (0.1-10 micrograms/ml) and then incubated with 5 mM sodium taurocholate. The synthetic activity of prostaglandins by cultured cells was assessed using 14C arachidonic acid prelabeled cells. Media content of prostaglandin E2 was assayed by radioimmunoassay. Cell viability was assayed by 51Cr release. Our results showed that arachidonic acid did not significantly protect cultured gastric cells against sodium taurocholate damage, while larger doses of arachidonic acid produced cell damage. Furthermore, cultured gastric cells produced mainly prostaglandin E2 and prostaglandin I2 and arachidonic acid stimulated prostaglandin E2 production dose-dependently (p less than 0.01). In conclusion, arachidonic acid does not directly protect gastric mucosal cells in vitro. In vivo protection by arachidonic acid must be based on indirect factors such as preservation of microvasculature.