scholarly journals Lipidomics Provides New Insight into Pathogenesis and Therapeutic Targets of the Ischemia—Reperfusion Injury

2021 ◽  
Vol 22 (6) ◽  
pp. 2798
Author(s):  
Zoran Todorović ◽  
Siniša Đurašević ◽  
Maja Stojković ◽  
Ilijana Grigorov ◽  
Slađan Pavlović ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Time Course ◽  
Membrane Lipids ◽  
Lipid Analysis ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Enzyme Inactivation ◽  
Critical Event ◽  
Tissue Ischemia ◽  
Insight Into

Lipids play an essential role in both tissue protection and damage. Tissue ischemia creates anaerobic conditions in which enzyme inactivation occurs, and reperfusion can initiate oxidative stress that leads to harmful changes in membrane lipids, the formation of aldehydes, and chain damage until cell death. The critical event in such a series of harmful events in the cell is the unwanted accumulation of fatty acids that leads to lipotoxicity. Lipid analysis provides additional insight into the pathogenesis of ischemia/reperfusion (I/R) disorders and reveals new targets for drug action. The profile of changes in the composition of fatty acids in the cell, as well as the time course of these changes, indicate both the mechanism of damage and new therapeutic possibilities. A therapeutic approach to reperfusion lipotoxicity involves attenuation of fatty acids overload, i.e., their transport to adipose tissue and/or inhibition of the adverse effects of fatty acids on cell damage and death. The latter option involves using PPAR agonists and drugs that modulate the transport of fatty acids via carnitine into the interior of the mitochondria or the redirection of long-chain fatty acids to peroxisomes.

scholarly journals Solvent selection for fatty acid residue analysis of archeologicial artifacts

2017 ◽  
Vol 3 (1) ◽  
pp. 1-10
Author(s):  
Jeffrey J. Rosentreter ◽  
John Malamakal ◽  
Kelli Barnes ◽  
Matt Alexander
Keyword(s):  
Fatty Acids ◽  
Extraction Efficiency ◽  
Lipid Analysis ◽  
Residue Analysis ◽  
Chemical Properties ◽  
Fatty Acid Residue ◽  
Quantitative Extraction ◽  
Selection For ◽  
Carbonized Wood ◽  
Insight Into

AbstractResidue analysis has rapidly become one of the most useful techniques for determining an artifact function and revealing insight into paleodiets. The success of analytical residue analysis often lies with the first preparatory step, where the residue is extracted from the object. Detection of a residue requires effective solvation of the material, and there is a large range of potential solvents. One purpose of this study is to determine the efficiency of various solvents for the extraction of fatty acids from charcoal, a material that is ubiquitous, easily identified, remarkably stable in the archaeological record but, most importantly for this research, retains fats extremely well. This investigation examines the removal efficiency of model fatty acids from carbonized wood samples. The strong affinity of lipids to charcoal makes carbonized wood ideal for retaining them, but also makes their extraction extremely challenging and thus an ideal benchmark for solvent extraction characterization. Several solvents (benzene, chloroform, hexane, methanol and water) are used to determine the quantitative extraction efficiency of tripalmitin. While benzene and chloroform perform best for some wood types, neither solvent is better for all carbonized wood. Correlations between the chemical properties of the solvents and the effectiveness of the extraction provide guidance for solvents. Findings indicate solvent characteristics including dipole moment, dielectric constant, hydrogen bonding, and molecular weight all play an important role in extraction of fat from a charcoal matrix. Results presented should provide guidelines to allow for more effective residue extration and more accurate lipid analysis.

Effects of ω-3 polyunsaturated fatty acids on cardiac sarcolemmal Na+/H+ exchange

2002 ◽  
Vol 283 (4) ◽  
pp. H1688-H1694 ◽  
Author(s):  
Danny P. Goel ◽  
Thane G. Maddaford ◽  
Grant N. Pierce
Keyword(s):  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Specific Effect ◽  
Eicosapentanoic Acid ◽  
Cardiac Membranes ◽  
Cardioprotective Effects ◽  
Myocardial Ischemia Reperfusion ◽  
Antiarrhythmic Actions

Myocardial ischemia-reperfusion activates the Na+/H+ exchanger, which induces arrhythmias, cell damage, and eventually cell death. Inhibition of the exchanger reduces cell damage and lowers the incidence of arrhythmias after ischemia-reperfusion. The ω-3 polyunsaturated fatty acids (PUFAs) are also known to be cardioprotective and antiarrhythmic during ischemia-reperfusion challenge. Some of the action of PUFAs may occur via inhibition of the Na+/H+ exchanger. The purpose of our study was to determine the capacity for selected PUFAs to alter cardiac sarcolemmal (SL) Na+/H+exchange. Cardiac membranes highly enriched in SL vesicles were exposed to 10–100 μM eicosapentanoic acid (EPA) or docosahexanoic acid (DHA). H+-dependent 22Na+ uptake was inhibited by 30–50% after treatment with ≥50 μM EPA or ≥25 μM DHA. This was a specific effect of these PUFAs, because 50 μM linoleic acid or linolenic acid had no significant effect on Na+/H+ exchange. The SL vesicles did not exhibit an increase in passive Na+ efflux after PUFA treatment. In conclusion, EPA and DHA can potently inhibit cardiac SL Na+/H+ exchange at physiologically relevant concentrations. This may explain, in part, their known cardioprotective effects and antiarrhythmic actions during ischemia-reperfusion.

In dialyzed squid axons oxidative stress inhibits the Na+/Ca2+ exchanger by impairing the Cai2+-regulatory site

2011 ◽  
Vol 301 (3) ◽  
pp. C687-C694 ◽  
Author(s):  
Reinaldo DiPolo ◽  
Luis Beaugé
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Peroxide ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Giant Axon ◽  
Tissue Ischemia ◽  
Major Mechanism ◽  
Intracellular Ca ◽  
Oxidant Production ◽  
Regulatory Sites

The Na+/Ca2+ exchanger, a major mechanism by which cells extrude calcium, is involved in several physiological and physiopathological interactions. In this work we have used the dialyzed squid giant axon to study the effects of two oxidants, SIN-1-buffered peroxynitrite and hydrogen peroxide (H2O2), on the Na+/Ca2+ exchanger in the absence and presence of MgATP upregulation. The results show that oxidative stress induced by peroxynitrite and hydrogen peroxide inhibits the Na+/Ca2+ exchanger by impairing the intracellular Ca2+ (Cai2+)-regulatory sites, leaving unharmed the intracellular Na+− and Ca2+−transporting sites. This effect is efficiently counteracted by the presence of MgATP and by intracellular alkalinization, conditions that also protect Hi+ and (Hi+ + Nai+) inhibition of Cai2+-regulatory sites. In addition, 1 mM intracellular EGTA reduces oxidant inhibition. However, once the effects of oxidants are installed they cannot be reversed by either MgATP or EGTA. These results have significant implications regarding the role of the Na+/Ca2+ exchanger in response to pathological conditions leading to tissue ischemia-reperfusion and anoxia/reoxygenation; they concur with a marked reduction in ATP concentration, an increase in oxidant production, and a rise in intracellular Ca2+ concentration that seems to be the main factor responsible for cell damage.

scholarly journals Arachidonic Acid Metabolism and Kidney Inflammation

2019 ◽  
Vol 20 (15) ◽  
pp. 3683 ◽  
Author(s):  
Tianqi Wang ◽  
Xianjun Fu ◽  
Qingfa Chen ◽  
Jayanta Kumar Patra ◽  
Dongdong Wang ◽  
...  
Keyword(s):  
Arachidonic Acid ◽  
Cytochrome P450 ◽  
Cell Membrane ◽  
Inflammatory Responses ◽  
Membrane Lipids ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Leukotriene B4 ◽  
P450 Monooxygenase ◽  
Wide Range

As a major component of cell membrane lipids, Arachidonic acid (AA), being a major component of the cell membrane lipid content, is mainly metabolized by three kinds of enzymes: cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP450) enzymes. Based on these three metabolic pathways, AA could be converted into various metabolites that trigger different inflammatory responses. In the kidney, prostaglandins (PG), thromboxane (Tx), leukotrienes (LTs) and hydroxyeicosatetraenoic acids (HETEs) are the major metabolites generated from AA. An increased level of prostaglandins (PGs), TxA2 and leukotriene B4 (LTB4) results in inflammatory damage to the kidney. Moreover, the LTB4-leukotriene B4 receptor 1 (BLT1) axis participates in the acute kidney injury via mediating the recruitment of renal neutrophils. In addition, AA can regulate renal ion transport through 19-hydroxystilbenetetraenoic acid (19-HETE) and 20-HETE, both of which are produced by cytochrome P450 monooxygenase. Epoxyeicosatrienoic acids (EETs) generated by the CYP450 enzyme also plays a paramount role in the kidney damage during the inflammation process. For example, 14 and 15-EET mitigated ischemia/reperfusion-caused renal tubular epithelial cell damage. Many drug candidates that target the AA metabolism pathways are being developed to treat kidney inflammation. These observations support an extraordinary interest in a wide range of studies on drug interventions aiming to control AA metabolism and kidney inflammation.

scholarly journals Morphogenesis and evolution mechanisms of bacterially-induced struvite

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Tian-Lei Zhao ◽  
Han Li ◽  
Hao-Fan Jiang ◽  
Qi-Zhi Yao ◽  
Ying Huang ◽  
...  
Keyword(s):  
Time Course ◽  
Carboxyl Groups ◽  
Precipitation Process ◽  
Phosphate Content ◽  
Biomimetic Mineralization ◽  
Struvite Precipitation ◽  
Growth Habits ◽  
Two Stages ◽  
Relevant Work ◽  
Insight Into

AbstractBacteria are able to induce struvite precipitation, and modify struvite morphology, leading to the mineral with various growth habits. However, the relevant work involving the morphogenesis is limited, thereby obstructing our understanding of bacterially mediated struvite mineralization. Here, an actinomycete Microbacterium marinum sp. nov. H207 was chosen to study its effect on struvite morphology. A combination of bacterial mineralization and biomimetic mineralization techniques was adopted. The bacterial mineralization results showed that strain H207 could induce the formation of struvite with grouping structure (i.e., a small coffin-like crystal grown on a large trapezoid-like substrate crystal), and the overgrowth structure gradually disappeared, while the substrate crystal further evolved into coffin-like, and quadrangular tabular morphology with time. The biomimetic experiments with different organic components confirmed that the soluble macromolecules rich in electronegative carboxyl groups secreted by strain H207 dominate the formation of the struvite grouping. The time-course biomimetic experiments with supernatant testified that the increase in pH and NH4+ content promoted the evolution of crystal habits. Moreover, the evolution process of substrate crystal can be divided into two stages. At the first stage, the crystal grew along the crystallographic b axis. At the later stage, coupled dissolution–precipitation process occurred, and the crystals grew along the corners (i.e., [110] and [1-10] directions). In the case of dissolution, it was also found that the (00-1) face of substrate crystal preferentially dissolved, which results from the low initial phosphate content and high PO43− density on this face. As a result, present work can provide a deeper insight into bio-struvite mineralization.

scholarly journals Repair cell first, then regenerate the tissues and organs

2021 ◽  
Vol 8 (1) ◽  
Author(s):  
Xiao-Bing Fu
Keyword(s):  
Tissue Repair ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Severe Trauma ◽  
Basic Unit ◽  
Basic Process ◽  
Tissue Repair And Regeneration ◽  
Healing Tissue ◽  
Organ Repair ◽  
And Function

AbstractWound healing, tissue repair and regenerative medicine are in great demand, and great achievements in these fields have been made. The traditional strategy of tissue repair and regeneration has focused on the level of tissues and organs directly; however, the basic process of repair at the cell level is often neglected. Because the cell is the basic unit of organism structure and function; cell damage is caused first by ischemia or ischemia-reperfusion after severe trauma and injury. Then, damage to tissues and organs occurs with massive cell damage, apoptosis and even cell death. Thus, how to achieve the aim of perfect repair and regeneration? The basic process of tissue or organ repair and regeneration should involve repair of cells first, then tissues and organs. In this manuscript, it is my consideration about how to repair the cell first, then regenerate the tissues and organs.

scholarly journals Time Course of Redox Biomarkers in COVID-19 Pneumonia: Relation with Inflammatory, Multiorgan Impairment Biomarkers and CT Findings

Antioxidants ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1126
Author(s):  
Tijana Kosanovic ◽  
Dragan Sagic ◽  
Vladimir Djukic ◽  
Marija Pljesa-Ercegovac ◽  
Ana Savic-Radojevic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Time Course ◽  
Redox Homeostasis ◽  
Original Data ◽  
Advanced Oxidation Protein Products ◽  
Oxidative Stress Parameters ◽  
Systemic Oxidative Stress ◽  
Dependent Relation ◽  
Organ Tissue ◽  
Insight Into

Although the original data on systemic oxidative stress in COVID-19 patients have recently started to emerge, we are still far from a complete profile of changes in patients’ redox homeostasis. We aimed to assess the extent of oxidative damage of proteins, lipids and DNA during the course of acute disease, as well as their association with CT pulmonary patterns. In order to obtain more insight into the origin of the systemic oxidative stress, the observed parameters were correlated with inflammatory biomarkers and biomarkers of multiorgan impairment. In this prospective study, we included 58 patients admitted between July and October 2020 with COVID-19 pneumonia. Significant changes in malondialdehyde, 8-hydroxy-2’-deoxyguanosine and advanced oxidation protein products levels exist during the course of COVID-19. Special emphasis should be placed on the fact that the pattern of changes differs between non-hospitalized and hospitalized individuals. Our results point to the time-dependent relation of oxidative stress parameters with inflammatory and multiorgan impairment biomarkers, as well as pulmonary patterns in COVID-19 pneumonia patients. Correlation between redox biomarkers and immunological or multiorgan impairment biomarkers, as well as pulmonary CT pattern, confirms the suggested involvement of neutrophils networks, IL-6 production, along with different organ/tissue involvement in systemic oxidative stress in COVID-19.

scholarly journals Lipid Metabolism Is Dysregulated before, during and after Pregnancy in a Mouse Model of Gestational Diabetes

2021 ◽  
Vol 22 (14) ◽  
pp. 7452
Author(s):  
Samuel Furse ◽  
Denise S. Fernandez-Twinn ◽  
Davide Chiarugi ◽  
Albert Koulman ◽  
Susan E. Ozanne
Keyword(s):  
Lipid Metabolism ◽  
Gestational Diabetes ◽  
Glucose Tolerance ◽  
Mouse Model ◽  
Time Course ◽  
De Novo ◽  
Lipid Analysis ◽  
Temporal Distribution ◽  
De Novo Lipogenesis ◽  
Analysis Tool

The aim of the current study was to test the hypothesis that maternal lipid metabolism was modulated during normal pregnancy and that these modulations are altered in gestational diabetes mellitus (GDM). We tested this hypothesis using an established mouse model of diet-induced obesity with pregnancy-associated loss of glucose tolerance and a novel lipid analysis tool, Lipid Traffic Analysis, that uses the temporal distribution of lipids to identify differences in the control of lipid metabolism through a time course. Our results suggest that the start of pregnancy is associated with several changes in lipid metabolism, including fewer variables associated with de novo lipogenesis and fewer PUFA-containing lipids in the circulation. Several of the changes in lipid metabolism in healthy pregnancies were less apparent or occurred later in dams who developed GDM. Some changes in maternal lipid metabolism in the obese-GDM group were so late as to only occur as the control dams’ systems began to switch back towards the non-pregnant state. These results demonstrate that lipid metabolism is modulated in healthy pregnancy and the timing of these changes is altered in GDM pregnancies. These findings raise important questions about how lipid metabolism contributes to changes in metabolism during healthy pregnancies. Furthermore, as alterations in the lipidome are present before the loss of glucose tolerance, they could contribute to the development of GDM mechanistically.

scholarly journals Heat stress elicits remodeling in the anther lipidome of peanut

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zolian S. Zoong Lwe ◽  
Ruth Welti ◽  
Daniel Anco ◽  
Salman Naveed ◽  
Sachin Rustgi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Heat Stress ◽  
Fatty Acid ◽  
Membrane Lipids ◽  
Fatty Acid Desaturase ◽  
Susceptible Genotype ◽  
Unsaturated Lipid ◽  
Lipid Species ◽  
Lipid Unsaturation ◽  
Fatty Acid Amount

AbstractUnderstanding the changes in peanut (Arachis hypogaea L.) anther lipidome under heat stress (HT) will aid in understanding the mechanisms of heat tolerance. We profiled the anther lipidome of seven genotypes exposed to ambient temperature (AT) or HT during flowering. Under AT and HT, the lipidome was dominated by phosphatidylcholine (PC), phosphatidylethanolamine (PE), and triacylglycerol (TAG) species (> 50% of total lipids). Of 89 lipid analytes specified by total acyl carbons:total carbon–carbon double bonds, 36:6, 36:5, and 34:3 PC and 34:3 PE (all contain 18:3 fatty acid and decreased under HT) were the most important lipids that differentiated HT from AT. Heat stress caused decreases in unsaturation indices of membrane lipids, primarily due to decreases in highly-unsaturated lipid species that contained 18:3 fatty acids. In parallel, the expression of Fatty Acid Desaturase 3-2 (FAD3-2; converts 18:2 fatty acids to 18:3) decreased under HT for the heat-tolerant genotype SPT 06-07 but not for the susceptible genotype Bailey. Our results suggested that decreasing lipid unsaturation levels by lowering 18:3 fatty-acid amount through reducing FAD3 expression is likely an acclimation mechanism to heat stress in peanut. Thus, genotypes that are more efficient in doing so will be relatively more tolerant to HT.

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