Reitmeyer J C, Peterson J W
Department of Microbiology, University of Texas Medical Branch, Galveston 77550.
Proc Soc Exp Biol Med. 1990 Mar;193(3):181-4. doi: 10.3181/00379727-193-43022.
Cholera toxin (CT) stimulated the release of arachidonic acid (AA) from Chinese hamster ovary cells with no apparent lag period. CT-induced release of [3H]AA or its metabolites was dose dependent during a 4-hr period of toxin exposure with a minimum effective dose of 0.1 ng/ml. CT-induced release of [3H]AA metabolites began within 15 min of toxin addition and became maximal after approximately 5 hr. Neither CT-A subunit nor CT-B subunit alone caused [3H]AA release. Furthermore, [3H]AA release was not caused by addition of dibutyryl cAMP to the culture medium, indicating that the observed effect of CT on arachidonate metabolism appeared to be independent of cAMP. The effect of CT on AA metabolism is proposed as a possible mechanism leading to the synthesis of prostaglandin E and fluid secretion during cholera.
霍乱毒素(CT)刺激中国仓鼠卵巢细胞释放花生四烯酸(AA),且无明显延迟期。在毒素暴露4小时期间,CT诱导的[3H]AA或其代谢产物的释放呈剂量依赖性,最小有效剂量为0.1 ng/ml。CT诱导的[3H]AA代谢产物的释放在添加毒素后15分钟内开始,并在约5小时后达到最大值。单独的CT-A亚基或CT-B亚基均未引起[3H]AA释放。此外,向培养基中添加二丁酰环磷腺苷(dibutyryl cAMP)不会导致[3H]AA释放,这表明CT对花生四烯酸代谢的观察到的作用似乎与环磷腺苷无关。CT对AA代谢的作用被认为是霍乱期间导致前列腺素E合成和液体分泌的一种可能机制。