phosphatidylethanol and Deficiency-Diseases

Previous reports have shown that selenium (Se) nutrition alters the lipoxygenase pathway and mitogenic responses in bovine lymphocytes. In order to further understand how Se may alter lymphocyte function, we examined the effects of Se nutrition on arachidonic acid (AA) metabolism and phospholipase D (PLD) activation. Lymphocytes were isolated from the lymph nodes of rats fed either Se-deficient diet (-Se) or Se-supplemented diet (+Se) for 12 weeks. Our results revealed that calcium ionophore A23187-stimulated lymphocytes derived from -Se rats produced significantly less prostaglandins (PGs) than those obtained from +Se rats. Phospholipase D (PLD) activation by 12-O-tetradecanoylphorbol-13-acetate (TPA) was significantly lower in lymphocytes obtained from -Se rats when compared to cells from +Se rats. Furthermore, the addition of PGE2, PGD2 or PGF2alpha to suspended lymphocytes from -Se rats significantly enhanced PLD activity. The effects of TPA and PGE2 on PLD activation were additive. However, the addition of PGE2 abolished the significant difference in PLD activation between -Se and +Se cells observed in response to TPA alone. Based on these results, we postulate that dietary Se status plays an important role in the regulation of AA metabolism that subsequently affects PLD activation.

Topics: Animals; Deficiency Diseases; Eicosanoids; Enzyme Activation; Glutathione Peroxidase; Glycerophospholipids; Humans; Jurkat Cells; Lymphocytes; Male; Phospholipase D; Prostaglandins; Rats; Rats, Long-Evans; Selenium; Signal Transduction; Tetradecanoylphorbol Acetate