Depletion Of Unsaturated Fatty Acids Research Articles

Soil organic carbon content and mineralization controlled by the composition, origin and molecular diversity of organic matter: A study in tropical alpine grasslands

The consensus for mechanisms controlling soil organic matter (SOM) persistence has shifted from traditional views based on SOM recalcitrance to a new paradigm based on SOM stabilization controlled by soil minerals and aggregates. Recent studies indicate that the origin, composition and molecular diversity of SOM are crucial to the decomposition and stabilization of SOM. However, it is not fully understood how the decomposition and stabilization of SOM are controlled at the molecular level. The objectives of this study were to investigate whether soil organic carbon (SOC) contents and mineralization are controlled by the composition, origin and molecular diversity of SOM. Soil samples were collected from contrasting bedrocks with different precipitation levels at tropical alpine grasslands of the Peruvian Andes. We applied a combination of a 76-day soil incubation experiment and pyrolysis-GC/MS assisted by thermochemolysis to investigate SOM decomposition and stabilization at the molecular level. The results indicated that soil samples with high SOC contents (92.6 ± 7.6 g kg−1 soil) and low SOC mineralization had abundant derivates of lignin, polysaccharides and n-alkanes. After the incubation, we observed neither a selective decomposition of any compound groups nor a decline of molecular diversity. In contrast, soil samples with low SOC contents (30.7 ± 2.8 g kg−1 soil) and higher SOC mineralization showed a depletion of plant-derived compounds, an accumulation of microbial-derived compounds and declined molecular diversity after the incubation. Furthermore, the SOC mineralization of these samples was positively correlated to the depletion of unsaturated fatty acids and the decrease in molecular diversity after the incubation. Therefore, we proposed that SOC contents and mineralization in our soils are (1) controlled by selective preservation of SOM molecular groups (e.g. plant-derived compounds), and (2) associated with changes in molecular diversity of SOM during microbial decomposition. Due to the selective preservation of organic compounds under different environmental conditions, we propose that environmental factors should be considered for the management of ecosystem services such as SOC sequestration in the studied region.

Selective stabilization of soil fatty acids related to their carbon chain length and presence of double bonds in the Peruvian Andes

Recent studies show increasing evidence for perseveration of soil organic matter (SOM) controlled by interactions with the soil matrix (i.e. mineral surfaces and aggregates) rather than chemical recalcitrance of the SOM. However, a consensus is still absent for potential controls of SOM chemical composition on SOM stabilization and persistence. Soil fatty acids (FAs), which form an important SOM component, can be used to investigate the effects of chemical properties on SOM stabilization because they are easily degraded by microorganisms but can be stabilized by the soil matrix against decomposition. Here we investigated whether inherent molecular properties of FAs control their stability in soils and their interactions with the soil matrix. Soil samples were collected from alpine grasslands of the Peruvian Andes (Andosols, Umbrisols and Phaeozems), as they are characterized by high carbon stocks and abundant aliphatics. We applied pyrolysis - gas chromatography/mass spectrometry analyses assisted by tetramethylammonium hydroxide (TMAH-pyrolysis-GC/MS) to determine the chemical composition of bulk SOM and FAs before and after a 76-day incubation experiment, comparing a situation with intact versus crushed soil aggregates. The results showed that the TMAH-pyrolysis-GC/MS yielded a large proportion of FAs (>60% relative abundance of identified compounds), with a major contribution of free FAs. FA stability was controlled by the presence of double bonds (unsaturated vs. saturated FAs) and carbon chain length. Unsaturated FAs significantly (P < 0.05) predicted soil organic carbon mineralization rates and were more depleted after the incubation compared to saturated FAs. The depletion of unsaturated FAs is likely explained by their easier degradation compared to saturated FAs. The easier degradation might be explained by the smaller extent of stabilization through association with mineral surfaces and/or chemical properties rather than stabilization through occlusion in aggregates. In terms of carbon chain length, FA stability decreased from short-chain to long-chain FAs. A possible explanation for this is that short-chain FAs received more protection by occlusion in aggregates compared to long-chain FAs or that short-chain FAs were produced during the incubation as a result of microbial transformation of FAs. Such microbial transformation has limited effects on the prediction of FA stability using double bonds and carbon chain length. However, we observed that soil types and horizons did influence the controls of double bonds and carbon chain length on FA stability. Our results corroborate the hypothesis that the inherent properties of soil FAs control their interactions with the soil matrix and indirectly govern their stabilization and persistence in the Peruvian Andean soils under study.

Pathological hypertrophy and cardiac dysfunction are linked to aberrant endogenous unsaturated fatty acid metabolism.

Pathological cardiac hypertrophy leads to derangements in lipid metabolism that may contribute to the development of cardiac dysfunction. Since previous studies, using high saturated fat diets, have yielded inconclusive results, we investigated whether provision of a high-unsaturated fatty acid (HUFA) diet was sufficient to restore impaired lipid metabolism and normalize diastolic dysfunction in the pathologically hypertrophied heart. Male, Wistar rats were subjected to supra-valvar aortic stenosis (SVAS) or sham surgery. After 6 weeks, diastolic dysfunction and pathological hypertrophy was confirmed and both sham and SVAS rats were treated with either normolipidic or HUFA diet. At 18 weeks post-surgery, the HUFA diet failed to normalize decreased E/A ratios or attenuate measures of cardiac hypertrophy in SVAS animals. Enzymatic activity assays and gene expression analysis showed that both normolipidic and HUFA-fed hypertrophied hearts had similar increases in glycolytic enzyme activity and down-regulation of fatty acid oxidation genes. Mass spectrometry analysis revealed depletion of unsaturated fatty acids, primarily linoleate and oleate, within the endogenous lipid pools of normolipidic SVAS hearts. The HUFA diet did not restore linoleate or oleate in the cardiac lipid pools, but did maintain body weight and adipose mass in SVAS animals. Overall, these results suggest that, in addition to decreased fatty acid oxidation, aberrant unsaturated fatty acid metabolism may be a maladaptive signature of the pathologically hypertrophied heart. The HUFA diet is insufficient to reverse metabolic remodeling, diastolic dysfunction, or pathologically hypertrophy, possibly do to preferentially partitioning of unsaturated fatty acids to adipose tissue.

Abstract 4115: Depletion of unsaturated fatty acids by stearoyl-coA desaturase inhibition results in endoplasmic reticulum stress-mediated tumor cell death

Abstract Over the past few years, a more detailed picture of the importance of metabolic pathways to the maintenance and progression of human cancers has begun to emerge. In particular, recent studies have implicated lipid biosynthesis and desaturation as a requirement for tumor cell survival. The endoplasmic reticulum-resident Stearoyl CoA Desaturase (SCD) is the rate limiting enzyme that catalyzes conversion of saturated fatty acids to monounsaturated fatty acids, a key step in the fatty acid metabolic network. In the studies reported here, we show that inhibition of SCD1 by siRNA or a small molecule antagonist results in strong induction of apoptosis and growth inhibition when tumor cells are cultured in reduced (2%) serum conditions but has little impact on cells cultured under normal (10%) serum conditions. Consistent with the observed dependence on SCD1, levels of SCD1 protein increased in response to decreasing serum levels. Both induction of SCD1 protein and sensitivity to growth inhibition by SCD1 inhibition could be reversed by supplementing growth media with unsaturated fatty acids. Transcription profiling of cells treated with an SCD inhibitor revealed strong induction of markers of endoplasmic reticulum stress. This finding was confirmed using siRNA specifically targeting SCD1. Underscoring its importance in cancer, SCD1 protein was found to be highly expressed in a large percentage of human cancer specimens. SCD inhibition resulted in tumor growth delay in a human gastric cancer xenograft model. Altogether, these results suggest that unsaturated fatty acids are required for tumor cell survival and that SCD may represent a viable target for the development of novel agents for cancer therapy. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 4115. doi:1538-7445.AM2012-4115

Effects of oleate-rich and linoleate-rich diets on the susceptibility of low density lipoprotein to oxidative modification in mildly hypercholesterolemic subjects.

We report the results of feeding oleate- or linoleate-enriched diets for 8 wk to mildly hypercholesterolemic subjects and the resulting alterations in composition and functional properties of their plasma LDL and HDL. LDL isolated from subjects on oleate-enriched diets was less susceptible to copper-mediated oxidation, as measured by conjugated diene and lipid peroxide formation, and less susceptible to LDL-protein modification, as evidenced by reduced LDL macrophage degradation after copper- or endothelial cell-induced oxidation. For all subjects, the percentage of 18:2 in LDL correlated strongly with the extent of conjugated diene formation (r = 0.89, P < 0.01) and macrophage degradation (r = 0.71, P < 0.01). Oxidation of LDL led to initial rapid depletion of unsaturated fatty acids in phospholipids followed by extensive loss of unsaturated fatty acids in cholesteryl esters and triglycerides. Changes in HDL fatty acid composition also occurred. However, HDL from both dietary groups retained its ability to inhibit oxidative modification of LDL. This study demonstrates that alterations in dietary fatty acid composition can effectively alter the fatty acid distribution of LDL and HDL in hypercholesterolemic subjects and that susceptibility to LDL oxidation is altered by these changes. Substitution of monounsaturated (rather than polyunsaturated) fatty acids for saturated fatty acids in the diet might be preferable for the prevention of atherosclerosis.

Membrane Deterioration in Senescing Carnation Flowers

The lipid fluidity of microsomal membranes from the petals of cut carnation flowers decreases as the flowers senesce. A comparable change in fluidity was induced by in vitro aging of microsomal membranes from young flowers under conditions in which membranous lipoxygenase-like activity was active. There was no change in fluidity when the membranes were aged in the presence of inhibitors of lipoxygenase or were heat-denatured prior to aging. Membranes from naturally senesced flowers and membranes that had been aged in vitro both sustained an increase in saturated:unsaturated fatty acid ratio that accounted for the decrease in lipid fluidity, and in both instances there was evidence for depletion of the unsaturated fatty acids, linoleic acid, and linolenic acid, which are substrates for lipoxygenase. Loss of lipid phosphate reflecting breakdown of membrane phospholipids preceded the depletion of unsaturated fatty acids attributable to the lipoxygenase-like activity. The data have been interpreted as indicating that fatty acid substrates for membrane-associated lipoxygenase-like activity are made available by the initiation of phospholipid degradation, and that the utilization of these substrates results in a selective depletion of unsaturated fatty acids from the membrane and an ensuing decrease in bulk lipid fluidity.

Mechanisms in 2-hexanone potentiation of chloroform hepatotoxicity

2-Hexanone (2-Hx) is known to potentiate chloroform (CHCl 3) hepatotoxicity in part by increasing the bioactivation of CHCl 3 to phosgene (COCl 2). Treatment of rats with 2-Hx + CHCl 3 in vivo did not initiate peroxidation of hepatic fatty acids as determined by formation of conjugated dienes or depletion of unsaturated fatty acids, or as determined by production of malondialdehyde (MDA) in vitro. A 5-fold decrease in the specific activity of succinate-dependent cytochrome c reductase in liver from rats treated in vivo with corn oil (vehicle) + CHCl 3 and in rats treated with 2-Hx + CHCl 3 indicated that a mechanism independent of CHCl 3 bioactivation may add to the hepatotoxic effects which result from the metabolism of chloroform to phosgene.

The effects of unsaturated fatty acid depletion on the proton permeability and energetic functions of yeast mitochondria.

1. The fatty acid composition of the ole-1 and ole-1 petite mutants of Saccharomyces cerevisiae was manipulated by growing the organism in the presence of defined supplements of Tween 80 or by allowing cells that had first been grown in the presence of Tween 80 to deplete their unsaturated fatty acids by sequent growth in the absence of Tween 80. 2. The transition temperature of Arrhenius plots of mitochondrial ATPase (adenosine triphosphatase) increases as the unsaturated fatty acid content is lowered. 3. Cells require larger amounts of unsaturated fatty acids to grow on ethanol at lower temperatures. 4. Cells that stop growing owing to unsaturated fatty acid depletion at low temperatures are induced to grow further by raising the temperature and this results in a further depletion of unsaturated acids. This is due to a higher rate, but not a greater efficiency, of mitochondrial ATP synthesis. 5. Arrhenius plots of the passive permeability of mitochondria to protons between 4 and 37 degrees C are linear. The rate and the Arrhenius activation energy of proton entry increase greatly as the unsaturated fatty acid content is lowered. 6. Unsaturated fatty acid depletion has the same effects on the proton permeability of ole-1 petite mitochondria, indicating that the mitochondrially synthesized subunits of the ATPase are not involved in the enhanced rates of proton entry. 7. The adenylate energy charge of depleted ole-1 cells is greatly decreased by growth on ethanol medium. 8. The adenylate energy charge of isolated mitochondria is also lowered by unsaturated fatty acid depletion. 9. The results confirm that unsaturated fatty acid depletion uncouples oxidative phosphorylation in yeast both in vivo and in vitro, and is a consequence of changes in the lipid part of the membrane.

Induction of respiratory incompetent mutants by unsaturated fatty acid depletion in [formula omitted

Constant levels of cellular unsaturated fatty acids were obtained by growing a fatty acid desaturase mutant of Saccharomyces cerevisiae in glucose limited chemostat cultures supplemented with various concentrations of Tween 80. An increase in the frequency of cytoplasmic respiratory incompetent mutants was observed in cultures growing at low cellular levels of unsaturated fatty acids. This effect has been shown to result from an increase in the rate of mutation as the cellular unsaturated fatty acid level is decreased. The majority of induced petite mutants are ϱ° (contain no mitochondrial DNA).

Biogenesis of mitochondria. The effects of altered membrane lipid composition on cation transport by mitochondria of Saccharomyces cerevisiae.

1. The fatty acid composition of the membrane lipids of a fatty acid desaturase mutant of Saccharomyces cerevisiae was manipulated by growing the organism in a medium containing defined fatty acid supplements. 2. Mitochondria were obtained whose fatty acids contain between 20% and 80% unsaturated fatty acids. 3. Mitochondria with high proportions of unsaturated fatty acids in their lipids have coupled oxidative phosphorylation with normal P/O ratios, accumulate K(+) ions in the presence of valinomycin and an energy source, and eject protons in an energy-dependent fashion. 4. If the unsaturated fatty acid content of the mitochondrial fatty acids is lowered to 20%, the mitochondria simultaneously lose active cation transport and the ability to couple phosphorylation to respiration. 5. The loss of energy-linked reactions is accompanied by an increased passive permeability of the mitochondria to protons. 6. Free fatty acids uncouple oxidative phosphorylation in yeast mitochondria and the effect is reversed by bovine serum albumin. 7. The free fatty acid contents of yeast mitochondria are unaffected by depletion of unsaturated fatty acids, and free fatty acids are not responsible for the uncoupling of oxidative phosphorylation in organelles depleted in unsaturated fatty acids. 8. It is suggested that the loss of energy-linked reactions in yeast mitochondria that are depleted in unsaturated fatty acids is a consequence of the increased passive permeability to protons, and is caused by a change in the physical properties of the lipid phase of the inner mitochondrial membrane.

Biogenesis of mitochondria. 19. The effects of unsaturated fatty acid depletion on the lipid composition and energy metabolism of a fatty acid desaturase mutant of Saccharomyces cerevisiae.

1. The lipid composition of a mutant ofSaccharomyces cerevisiae which cannot synthesize unsaturated fatty acid (UFA) can be extensively manipulated by growing the organism in the presence of added fatty acids. 2. Growth of the mutant is supported by a wide range of unsaturated fatty acids including oleic, palmitoleic, petroselenic, 11-eicosaenoic, ricinoleic, arachidonic, clupanodonic, linoleic and linolenic acids; 9- and 10-hydroxystearic acids support growth less effectively, but erucic, nervonic, elaidic and saturated fatty acids (C8∶0−C20∶0)* are ineffective. All the fatty acids which support growth are incorporated into cell lipids, apparently without further metabolism. 3. The effects of altered lipid composition on the energy metabolism of yeast cells were investigated. Cells containing less than approximately 20% of their fatty acids as UFA cannot grow on non-fermentable substrates, and their growth on glucose is restricted to that which can be supported by fermentation alone. 4. UFA-depleted cells contain mitochondria which are apparently normal in morphology, furthermore they have normal levels of cytochromesa+a3,b,c1 andc and respire at normal rates. This suggests that the lesion in energy metabolism produced by UFA-depletion may be the loss of the ability of the mitochondria to couple respiration to phosphorylation. 5. UFA-depleted cells incorporate added UFA into their cell lipids and subsequently regain the ability to grow on non-fermentable substrates, showing that the lesion in energy metabolism is fully reversible.

The effects of depletion of unsaturated fatty acids on the energy-dependent reactions of yeast mitochondria.

Research Article| June 01 1971 The effects of depletion of unsaturated fatty acids on the energy-dependent reactions of yeast mitochondria J M Haslam J M Haslam Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1971) 123 (2): 6P–7P. https://doi.org/10.1042/bj1230006Pb Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation J M Haslam; The effects of depletion of unsaturated fatty acids on the energy-dependent reactions of yeast mitochondria. Biochem J 1 June 1971; 123 (2): 6P–7P. doi: https://doi.org/10.1042/bj1230006Pb Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1971 London: The Biochemical Society1971 Article PDF first page preview Close Modal You do not currently have access to this content.

Specific effect of unsaturated fatty acid depletion on mitochondrial oxidative phosphorylation in [formula omitted

A mutant of Saccharomyces cerevisiae which cannot synthesise unsaturated fatty acid (UFA) was used to investigate the role of UFA in yeast metabolism. UFA depleted cells contained cytochromes and respired at normal rates, but could not grow on non-fermentable substrate, and their growth on glucose was restricted to that which could be supported by fermentation alone. Isolated mitochondria lacked respiratory control and had negligible phosphorylation. Thus UFA depletion leads to the specific loss of mitochondrial oxidative phosphorylation by S. cerevisiae both in vivo and in vitro .