Synthesis and polymorphic phase behaviour of polyunsaturated phosphatidylcholines and phosphatidylethanolamines

Dekker, Carien; Kessel, W.S.M. Geurts van; Klomp, J.; Pieters, J.; Kruijff, Ben de

doi:10.1016/0009-3084(83)90012-9

Cited by 103 publications

(52 citation statements)

References 18 publications

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“…In this study, we found that gamma-ray radiation induced an instantaneous increase in the levels of intracellular ROS within minutes, a mitochondrial dysfunction within hours, and a persistent increase of mitochondrial ROS levels and oxidation of mitochondrial DNA within [15,16]. These phospholipids are located in the inner mitochondrial membrane and are required for the optimum activity of ETC complexes, including complexes I and III [34,35].…”

Section: Discussionmentioning

confidence: 95%

“…The mitochondrial inner membrane contains phospholipids, such as phosphatidylcholine, phosphatidylethanolamine, and cardiolipin, which play very important roles in the optimal functioning of numerous enzymes involved in the ETC of mitochondria [15,16]. Alterations in the membrane lipid profile, such as a decrease in lipid content, peroxidation, and changes in composition may result in or enhance the generation of O 2 -arising from leakage of electrons from ETC component enzymes.…”

Section: Thesementioning

confidence: 99%

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Mitochondrial dysfunction, a probable cause of persistent oxidative stress after exposure to ionizing radiation

Yoshida

Goto

Kawakatsu

et al. 2012

Free Radical Research

150

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Several recent studies have suggested that the reactive oxygen species (ROS) generated from mitochondria contribute to genomic instability after exposure of the cells to ionizing radiation, but the mechanism of this process is not yet fully understood. We examined the hypothesis that irradiation induces mitochondrial dysfunction to cause persistent oxidative stress, which contributes to genomic instability. After the exposure of cells to 5 Gy gamma-ray irradiation, we found that the irradiation induced the following changes in a clear pattern of time courses. First, a robust increase of intracellular ROS levels occurred within minutes, but the intracellular ROS disappeared within 30 minutes. Then the mitochondrial dysfunction was detected at 12 hours after irradiation, as indicated by the decreased activity of NADH dehydrogenase (Complex I), the most important enzyme in regulating the release of ROS from the mitochondrial electron transport chain (ETC). Finally, a significant increase of ROS levels in the mitochondria and the oxidation of mitochondrial DNA were observed in cells at 24 hours or later after irradiation.Although further experiments are required, results in this study support the hypothesis that mitochondrial dysfunction causes persistent oxidative stress that may contribute to promote radiation-induced genomic instability.2

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Section: Discussionmentioning

confidence: 95%

Section: Thesementioning

confidence: 99%

Mitochondrial dysfunction, a probable cause of persistent oxidative stress after exposure to ionizing radiation

Yoshida

Goto

Kawakatsu

et al. 2012

Free Radical Research

150

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“…An illustrative example is the suppression of the bilayer to inverse hexagonal phase transition occurs with increasing unsaturation from PE 16 : 0/18 : 1 (L a to H II ¼ 758C) with one unsaturated bond, to PE 18 : 3/18 : 3 (L a to H II ¼ 2 258C) with six unsaturated bonds, to PE 20 : 4/20 : 4 (L a to H II ¼ 2 308C) with eight unsaturated bonds [46]. We note that we have not included overall chain length, or the position of the unsaturation, in our calculations.…”

Section: Assumptions Used To Constrain the Search For A Universal Pivmentioning

confidence: 99%

Anin vivoratio control mechanism for phospholipid homeostasis: evidence from lipidomic studies

Dymond

hague

Postle

et al. 2013

J. R. Soc. Interface.

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While it is widely accepted that the lipid composition of eukaryotic membranes is under homeostatic control, the mechanisms through which cells sense lipid composition are still the subject of debate. It has been postulated that membrane curvature elastic energy is the membrane property that is regulated by cells, and that lipid composition is maintained by a ratio control function derived from the concentrations of type II and type 0 lipids, weighted appropriately. We assess this proposal by seeking a signature of ratio control in quantified lipid composition data obtained by electrospray ionization mass spectrometry from over 40 independent asynchronous cell populations. Our approach revealed the existence of a universal 'pivot' lipid, which marks the boundary between type 0 lipids and type II lipids, and which is invariant between different cell types or cells grown under different conditions. The presence of such a pivot species is a distinctive signature of the operation in vivo, in human cell lines, of a control function that is consistent with the hypothesis that membrane elastic energy is homeostatically controlled.

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“…Moreover, arachidonic acid (C 20:4 fatty acid) esterified in phosphatidylethanolamine, which has a small head group area, promotes highly negative membrane curvature (18). If the supply of very-long-chain fatty acids becomes limiting, as is proposed to occur in acc1-7-1, one might therefore predict that the membrane bend would become more and more unstable (illustrated in Fig.…”

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confidence: 99%

A Yeast Acetyl Coenzyme A Carboxylase Mutant Links Very-Long-Chain Fatty Acid Synthesis to the Structure and Function of the Nuclear Membrane-Pore Complex

Schneiter

Hitomi

Ivessa

et al. 1996

Molecular and Cellular Biology

183

185

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The conditional mRNA transport mutant of Saccharomyces cerevisiae, acc1-7-1 (mtr7-1), displays a unique alteration of the nuclear envelope. Unlike nucleoporin mutants and other RNA transport mutants, the intermembrane space expands, protuberances extend from the inner membrane into the intermembrane space, and vesicles accumulate in the intermembrane space. MTR7 is the same gene as ACC1, encoding acetyl coenzyme A (CoA) carboxylase (Acc1p), the rate-limiting enzyme of de novo fatty acid synthesis. Genetic and biochemical analyses of fatty acid synthesis mutants and acc1-7-1 indicate that the continued synthesis of malonyl-CoA, the enzymatic product of acetyl-CoA carboxylase, is required for an essential pathway which is independent from de novo synthesis of fatty acids. We provide evidence that synthesis of very-long-chain fatty acids (C 26 atoms) is inhibited in acc1-7-1, suggesting that very-long-chain fatty acid synthesis is required to maintain a functional nuclear envelope.The regulation of synthesis and transport of phospholipids has been characterized at length, but the signals which determine the phospholipid and fatty acid composition of particular membranes and membrane-specific lipid requirements are not well understood (7,62,81,83). The present investigation, which is the outgrowth of analysis of a yeast (Saccharomyces cerevisiae) mutant which accumulates poly(A) ϩ RNA in the nucleus at the restrictive temperature (41), documents a critical relationship between fatty acid chain length and the integrity of the nuclear membrane and nuclear pore complex (NPC).The biosynthesis of very-long-chain fatty acids requires four enzyme systems: acetyl coenzyme A (CoA) carboxylase, fatty acid synthase, fatty acid desaturase, and the fatty acyl chain elongation system (Fig. 1). The rate-limiting step of the de novo synthesis of fatty acids is under control of the first of these, acetyl-CoA carboxylase (Acc1p; EC 6.4.1.2). This biotinylated enzyme catalyzes the ATP-dependent carboxylation of acetyl-CoA to yield malonyl-CoA, which serves as the twocarbon-unit donor for the subsequent synthesis of long-chain fatty acids by the fatty acid synthase complex. The chain length of newly synthesized fatty acids appears to depend on the concentration of malonyl-CoA rather than on the activity of the fatty acid synthase complex (35, 43a, 82). Acc1p thus regulates both the overall rate of de novo synthesis and chainlength distribution of long-chain fatty acids. It is perhaps for this reason that its activity is subject to complex regulation (48). Yeast Acc1p/Fas3p has a subunit molecular mass of 250 kDa, is active as a tetramer, and is subject to short-term regulation by phosphorylation (2, 60, 90). Its transcription is positively regulated by Ino2p and Ino4p and negatively regulated by Opi1p; i.e., it is under the general control of phospholipid synthesis (14, 31).Many yeast long-chain fatty acid auxotrophs have been isolated (72). Sixty-one are alleles of acc1 (55, 67), while others bear mutations in fatty acid synthase (19,...

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Synthesis and polymorphic phase behaviour of polyunsaturated phosphatidylcholines and phosphatidylethanolamines

Cited by 103 publications

References 18 publications

Mitochondrial dysfunction, a probable cause of persistent oxidative stress after exposure to ionizing radiation

Mitochondrial dysfunction, a probable cause of persistent oxidative stress after exposure to ionizing radiation

Anin vivoratio control mechanism for phospholipid homeostasis: evidence from lipidomic studies

A Yeast Acetyl Coenzyme A Carboxylase Mutant Links Very-Long-Chain Fatty Acid Synthesis to the Structure and Function of the Nuclear Membrane-Pore Complex

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