Lambert I H
Institute of Biological Chemistry A, August Krogh Institute, University of Copenhagen, Denmark.
J Membr Biol. 1987;98(3):207-21. doi: 10.1007/BF01871184.
Arachidonic acid inhibits the cell shrinkage observed in Ehrlich ascites tumor cells during regulatory volume decrease (RVD) or after addition of the Ca ionophore A23187 plus Ca. In Na-containing media, arachidonic acid increases cellular Na uptake under isotonic as well as under hypotonic conditions. Arachidonic acid also inhibits KCl and water loss following swelling in Na-free, hypotonic media even when a high K conductance has been ensured by addition of gramicidin. In isotonic, Na-free medium arachidonic acid inhibits A23187 + Ca-induced cell shrinkage in the absence but not in the presence of gramicidin. It is proposed that inhibition of RVD in hypotonic media by arachidonic acid is caused by reduction in the volume-induced Cl and K permeabilities as well as by an increase in Na permeability and that reduction in A23187 + Ca-induced cell shrinkage is due to a reduction in K permeability and an increase in Na permeability. The A23187 + Ca-activated Cl permeability in unaffected by arachidonic acid. PGE2 inhibits RVD in Na-containing, hypotonic media but not in Na-free, hypotonic media, indicating a PGE2-induced Na uptake. PGE2 has no effect on the volume-activated K and Cl permeabilities. LTB4, LTC4 and LTE4 inhibit RVD insignificantly in hypotonically swollen cells. LTD4, moreover, induces cell shrinkage in steady-state cells and accelerates the RVD following hypotonic exposure. The effect of LTD4 even reflects a stimulating effect on K and Cl transport pathways. Thus none of the leukotrienes show the inhibitory effect found for arachidonic acid on the K and Cl permeabilities. The RVD response in hypotonic, Na-free media is, on the other hand, also inhibited by addition of the unsaturated oleic, linoleic, linolenic and palmitoleic acid, even in the presence of the cationophor gramicidin. The saturated arachidic and stearic acid had no effect on RVD. It is, therefore, suggested that a minor part of the inhibitory effect of arachidonic acid on RVD in Na-containing media is via an increased synthesis of prostaglandins and that the major part of the arachidonic acid effect on RVD in Na-free media, and most probably also in Na-containing media, is due to the inhibition of the volume-induced K and Cl transport pathways, caused by a nonspecific detergent effect of an unsaturated fatty acid.
花生四烯酸可抑制艾氏腹水瘤细胞在调节性容积减小（RVD）过程中或添加钙离子载体A23187加钙离子后所观察到的细胞皱缩。在含钠培养基中，花生四烯酸在等渗和低渗条件下均会增加细胞对钠的摄取。即使在添加短杆菌肽确保高钾电导的情况下，花生四烯酸也能抑制在无钠、低渗培养基中肿胀后的氯化钾和水分流失。在等渗、无钠培养基中，花生四烯酸在不存在短杆菌肽时可抑制A23187 + 钙离子诱导的细胞皱缩，但在存在短杆菌肽时则不能。有人提出，花生四烯酸对低渗培养基中RVD的抑制作用是由于容积诱导的氯离子和钾离子通透性降低以及钠离子通透性增加所致，而A23187 + 钙离子诱导的细胞皱缩的减少是由于钾离子通透性降低和钠离子通透性增加所致。花生四烯酸不影响A23187 + 钙离子激活的氯离子通透性。前列腺素E2（PGE2）可抑制含钠低渗培养基中的RVD，但不能抑制无钠低渗培养基中的RVD，这表明PGE2可诱导钠摄取。PGE2对容积激活的钾离子和氯离子通透性无影响。白三烯B4（LTB4）、白三烯C4（LTC4）和白三烯E4（LTE4）对低渗肿胀细胞中RVD的抑制作用不明显。此外，白三烯D4（LTD4）可诱导稳态细胞皱缩，并加速低渗暴露后的RVD。LTD4的作用甚至反映出对钾离子和氯离子转运途径的刺激作用。因此，没有一种白三烯表现出花生四烯酸对钾离子和氯离子通透性所具有的抑制作用。另一方面，即使在存在阳离子载体短杆菌肽的情况下，添加不饱和的油酸、亚油酸、亚麻酸和棕榈油酸也会抑制无钠低渗培养基中的RVD反应。饱和的花生酸和硬脂酸对RVD无影响。因此，有人认为花生四烯酸对含钠培养基中RVD的抑制作用的一小部分是通过增加前列腺素的合成实现的，而花生四烯酸对无钠培养基中RVD的影响的主要部分，很可能在含钠培养基中也是如此，是由于不饱和脂肪酸的非特异性去污剂作用导致容积诱导的钾离子和氯离子转运途径受到抑制所致。
