Molecular species of membrane phospholipids containing arachidonic acid and linoleic acid contribute to the interindividual variability of red blood cell Na+-Li+ countertransport: In vivo and in vitro evidence

Abstract

Previous studies indicate a particular sensitivity of red blood cell Na(+)-Li+ countertransport activity to small variations in the fatty acid composition of membrane phospholipids. To assess whether the interindividual variability of Na(+)-Li+ countertransport is related to differences in the species pattern of erythrocyte phosphatidylcholine (PC) and phosphatidylethanolamine (PE) in vivo, the molecular species composition of PC and PE as well as the kinetics of Na(+)-Li+ countertransport were analyzed in parallel in normo- and hyperlipidemic donors. Both in diacyl-PC and in diacyl-PE the species 16:0/20:4 and 16:0/18:2 were, respectively, positively and negatively related to the apparent maximal velocity of Na(+)-Li+ countertransport. The sum of all species with 20:4 at sn2 of diacyl-PE exhibited a strong positive (r = 0.82, 2p < 0.001), and those containing 18:2 a negative correlation (r = -0.63, 2p < 0.01) to the transport activity. Essentially similar connections were observed between these species and the apparent affinity of the transport system for intracellular Na+. To evaluate whether the associations between molecular species of membrane phospholipids and Na(+)-Li+ countertransport activity were indicative of a causal relationship, the species 16:0/20:4-PC and 16:0/18:2-PC were selectively introduced into the erythrocyte membrane by means of the PC-specific transfer protein. Replacement of 11% of native PC by 16:0/18:2-PC inhibited the transport rate by about 25%. Exchange of 6 and 9% of PC with 16:0/20:4-PC, in contrast, accelerated the transport rate by 30 and 60%, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Delayed oxidative degradation of polyunsaturated diacyl phospholipids in the presence of plasmalogen phospholipids in vitro

“…Molecular species analysis of phospholipids was performed by phospholipase C treatment of phospholipids, derivatization of diradylglycerols with 2,3-dinitrobenzoylchloride, separation of individual species by HPLC and detection of the absorbance of the peaks at 254 nm as described in detail previously [21,22].…”

Salt Loading Increases Urinary Excretion of Linoleic Acid Diols and Triols in Healthy Human Subjects

“…Clinical studies have shown that an increase in dietary intake of LA inhibits red and white blood cell Na ϩ /Li ϩ countertransport and reduces BP. [1][2][3][4][5][6][7]10 In addition, in vitro studies have demonstrated that LA metabolites inhibit cardiac sodium channels. 19,20 Several studies in rats have shown the development of salt-sensitive hypertension with the inability to excrete an acute salt load after dietary LA acid deprivation that is corrected by administration of LA, suggesting that LA is intimately involved with renal sodium handling.…”

“…Increased dietary LA intake reduces systolic blood pressure, increases red blood cell membrane LA content, and alters red and white blood cell sodium transport processes in clinical studies. [1][2][3][4][5][6][7] Conversely, dietary LA deprivation in rats results in the development of salt-sensitive hypertension and an inability to excrete an acute salt load, with both effects reversed by the administration of LA. 8 -10 LA is a precursor of arachidonic acid, and it has been proposed that the effects of LA on blood pressure and salt excretion may be mediated through the production of various cytochrome P450 (CYP) eicosanoids and/or prostaglandins, including the epoxyeicosatrienoic acids (EETs) [11][12][13][14] and the prostacyclin metabolite 6-keto-prostaglandin (PG) F1␣.…”

Kinetic characteristics of the erythrocyte sodium-lithium countertransporter in black normotensive subjects compared with three other ethnic groups

“…The sodium-lithium countertransporter has been shown to be sensitive to membrane fatty acid composition. 36,37 The lower plasma triglyceride concentrations in the black subjects could reflect subtle differences in the fatty acid composition of their triglycerides and these might be mirrored in the fatty acid composition of the cell membranes, producing a different behavioural pattern for the countertransporter. Certainly the fatty acid composition of adipose tissue has been shown to be altered in blacks compared to Caucasian subjects, 38 with differences in the key fats such as stearic acid, a fatty acid known to influence countertransport behaviour.…”

“…Certainly the fatty acid composition of adipose tissue has been shown to be altered in blacks compared to Caucasian subjects, 38 with differences in the key fats such as stearic acid, a fatty acid known to influence countertransport behaviour. 36,37 The observed difference in the behaviour of the sodium-lithium countertransporter in a single ethnic group suggests that this phenomenon may be genetically determined. SLC activity has long been known to be under genetic influence, 9,19,20,26 while both V max and k Na have shown familial associations.…”