N-Acylphosphatidylethanolamine Accumulation in Potato Cells upon Energy Shortage Caused by Anoxia or Respiratory Inhibitors

Abstract

A minor phospholipid was isolated from potato (Solanum tuberosum L. cv Bintje) cells, chromatographically purified, and identified by electrospray ionization mass spectrometry as N-acylphosphatidylethanolamine (NAPE). The NAPE level was low in unstressed cells (13 Ϯ 4 nmol g fresh weight Ϫ1 ). According to acyl chain length, only 16/18/18 species (group II) and 18/18/18 species (group III) were present. NAPE increased up to 13-fold in anoxia-stressed cells, but only when free fatty acids (FFAs) started being released, after about 10 h of treatment. The level of groups II and III was increased by unspecific N-acylation of phosphatidylethanolamine, and new 16/16/18 species (group I) appeared via N-palmitoylation. NAPE also accumulated in aerated cells treated with NaN 3 plus salicylhydroxamate. N-acyl patterns of NAPE were dominated by 18:1, 18:2, and 16:0, but never reflected the FFA composition. Moreover, they did not change greatly after the treatments, in contrast with O-acyl patterns. Anoxia-induced NAPE accumulation is rooted in the metabolic homeostasis failure due to energy deprivation, but not in the absence of O 2 , and is part of an oncotic death process. The acyl composition of basal and stress-induced NAPE suggests the existence of spatially distinct FFA and phosphatidylethanolamine pools. It reflects the specificity of NAPE synthase, the acyl composition, localization and availability of substrates, which are intrinsic cell properties, but has no predictive value as to the type of stress imposed. Whether NAPE has a physiological role depends on the cell being still alive and its compartmentation maintained during the stress period.

Phosphatidic Acid and N-Acylphosphatidylethanolamine Form Membrane Domains in Escherichia coli Mutant Lacking Cardiolipin and Phosphatidylglycerol

“…N-Acyl-PE serves as the precursor to a class of bioactive lipids called N-acylethanolamines, which are produced in a variety of tissues and implicated in the modulation of pain sensation, feeding, and sleep cycles (49, 50, 51 and references within). Both in animal tissues and plants N-acyl-PE accumulates under stress conditions and plays a dual role, as a direct precursor for N-acylethanolamine signaling pathways and as a stabilizing component of the membrane (49,52). Pathways of biosynthesis and function of N-acyl-PE in E. coli cells remain to be studied.…”

A liquid chromatography–tandem mass spectrometry method for measurement of N-modified phosphatidylethanolamines

“…NAPEs have been previously directly measured by two methods: TLC [26] and mass spectrometry [2; 26; 27; 28; 29]. While TLC is readily available and inexpensive, it lacks specificity for individual N -acyl chains and is less sensitive and more difficult to accurately quantify than mass spectrometry methods.…”

N-Acylethanolamines Are Metabolized by Lipoxygenase and Amidohydrolase in Competing Pathways during Cottonseed Imbibition

“…As an alternative, some polyunsaturated NAEs are metabolized by 13-LOX and 13-AOS to yield NAE oxylipins (13-hydroperoxy NAE, 13-hydroperoxy octadecadienoylethanolamine and 12-oxo-13-hydroxy NAE, 12-oxo-13-hydroxy octadecenoylethanolamine). FFAs formed from hydrolysis of NAE or glycerophospholipids can be incorporated directly into the N-position of NAPE (Chapman, 2000;Rawyler and Braendle, 2001) by NAPE synthase. This overall cycle could be used for signal transduction (formation of NAE lipid mediators) or to scavenge FFAs (for membrane protection) depending upon cellular demands.…”