scholarly journals Cardiolipin, Perhydroxyl Radicals, and Lipid Peroxidation in Mitochondrial Dysfunctions and Aging

2020 ◽  
Vol 2020 ◽  
pp. 1-14 ◽  
Author(s):  
Alexander V. Panov ◽  
Sergey I. Dikalov
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Direct Oxidation ◽  
Inner Mitochondrial Membrane ◽  
Mitochondrial Dysfunctions ◽  
Functional Integrity ◽  
Oxidative Damages ◽  
Specific Localization ◽  
Perhydroxyl Radical

Mitochondrial dysfunctions caused by oxidative stress are currently regarded as the main cause of aging. Accumulation of mutations and deletions of mtDNA is a hallmark of aging. So far, however, there is no evidence that most studied oxygen radicals are directly responsible for mutations of mtDNA. Oxidative damages to cardiolipin (CL) and phosphatidylethanolamine (PEA) are also hallmarks of oxidative stress, but the mechanisms of their damage remain obscure. CL is the only phospholipid present almost exclusively in the inner mitochondrial membrane (IMM) where it is responsible, together with PEA, for the maintenance of the superstructures of oxidative phosphorylation enzymes. CL has negative charges at the headgroups and due to specific localization at the negative curves of the IMM, it creates areas with the strong negative charge where local pH may be several units lower than in the surrounding bulk phases. At these sites with the higher acidity, the chance of protonation of the superoxide radical (O2•), generated by the respiratory chain, is much higher with the formation of the highly reactive hydrophobic perhydroxyl radical (HO2•). HO2• specifically reacts with the double bonds of polyunsaturated fatty acids (PUFA) initiating the isoprostane pathway of lipid peroxidation. Because HO2• is formed close to CL aggregates and PEA, it causes peroxidation of the linoleic acid in CL and also damages PEA. This causes disruption of the structural and functional integrity of the respirosomes and ATP synthase. We provide evidence that in elderly individuals with metabolic syndrome (MetS), fatty acids become the major substrates for production of ATP and this may increase several-fold generation of O2• and thus HO2•. We conclude that MetS accelerates aging and the mitochondrial dysfunctions are caused by the HO2•-induced direct oxidation of CL and the isoprostane pathway of lipid peroxidation (IPLP). The toxic products of IPLP damage not only PEA, but also mtDNA and OXPHOS proteins. This results in gradual disruption of the structural and functional integrity of mitochondria and cells.

scholarly journals Narrative Review of n-3 Polyunsaturated Fatty Acid Supplementation upon Immune Functions, Resolution Molecules and Lipid Peroxidation

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 662
Author(s):  
Gary P. Zaloga
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Fish Oil ◽  
Inflammatory Responses ◽  
Biological Effects ◽  
Scientific Evidence ◽  
Immune Functions ◽  
Pufa Supplementation ◽  
Fish Oil Supplementation

Fish oil supplementation is commonplace in human nutrition and is being used in both enteral and parenteral formulations during the treatment of patients with a large variety of diseases and immune status. The biological effects of fish oil are believed to result from their content of n-3 polyunsaturated fatty acids (PUFA), particularly docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA). These fatty acids are known to have numerous effects upon immune functions and are described as immunomodulatory. However, immunomodulatory is a nondescript term that encompasses immunostimulation and immunosuppression. The primary goal of this review is to better describe the immune effects of n-3 PUFA as they relate to immunostimulatory vs. immunosuppressive effects. One mechanism proposed for the immune effects of n-3 PUFA relates to the production of specialized pro-resolving mediators (SPMs). A second goal of this review is to evaluate the effects of n-3 PUFA supplementation upon production of SPMs. Although n-3 PUFA are stated to possess anti-oxidative properties, these molecules are highly oxidizable due to multiple double bonds and may increase oxidative stress. Thus, the third goal of this review is to evaluate the effects of n-3 PUFA upon lipid oxidation. We conclude, based upon current scientific evidence, that n-3 PUFA suppress inflammatory responses and most cellular immune responses such as chemotaxis, transmigration, antigen presentation, and lymphocyte functions and should be considered immunosuppressive. n-3 PUFA induced production of resolution molecules is inconsistent with many resolution molecules failing to respond to n-3 PUFA supplementation. n-3 PUFA supplementation is associated with increased lipid peroxidation in most studies. Vitamin E co-administration is unreliable for prevention of the lipid peroxidation. These effects should be considered when administering n-3 PUFA to patients that may be immunosuppressed or under high oxidative stress due to illness or other treatments.

scholarly journals Hyperglycemia and Hyperlipidemia Induced Inflammation and Oxidative Stress in Human T Lymphocytes and Salutary Effects of ω- 3 Fatty Acid.

2020 ◽  
pp. 1-9
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
T Cells ◽  
Fatty Acid ◽  
T Lymphocytes ◽  
Palmitic Acid ◽  
Linolenic Acid ◽  
High Glucose ◽  
Human T Lymphocytes

Abstract Type 2 Diabetes conditions are associated with hyperglycemia and hyperlipidemia; however, the role of Saturated Fatty Acids (SFA) vs. Unsaturated Fatty Acids (UFA) and high glucose on human T lymphocytes (T cells) is not known. We investigated the salutary effect of the UFA ω-3 fatty acid, α- linolenic acid, on glucose and SFA, palmitic acid, induced activation on T cells as a cause of the inflammatory process with high glucose and SFA foods. These cells in the presence of palmitic acid and/or high glucose but not linolenic acid exhibited a concentration and time-dependent emergence of insulin receptors (INSR), expression, generation of ROS, lipid peroxidation, cytokines and NF-kB p65 translocation to the nucleus. Whereas, activation of the cells by elevated levels of glucose and palmitic acid were additive, addition of linolenic acid in a dose-related manner inhibited activation of cells by glucose and palmitic acid and reduced markers of oxidative stress, lipid peroxidation and cytokines. We propose that UFAs such as α-linolenic acid may serve as a protective mechanism against the deleterious effects of hyperglycemia and hyperlipidemia of high sugar and SFA foods as in diabetes.

Saccharomyces cerevisiae strain expressing a plant fatty acid desaturase produces polyunsaturated fatty acids and is susceptible to oxidative stress induced by lipid peroxidation

2006 ◽  
Vol 40 (5) ◽  
pp. 897-906 ◽  
Author(s):  
Ana Cipak ◽  
Meinhard Hasslacher ◽  
Oksana Tehlivets ◽  
Emma J. Collinson ◽  
Morana Zivkovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Saccharomyces Cerevisiae ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Fatty Acid ◽  
Polyunsaturated Fatty Acids ◽  
Fatty Acid Desaturase

Effect of increased levels of dietary alpha-linolenic acid on the n-3 polyunsaturated fatty acid bioavailability and oxidative stress in rat

2021 ◽  
pp. 1-43
Author(s):  
Leslie Couëdelo ◽  
Benjamin Buaud ◽  
Hélène Abrous ◽  
Ikram Chamekh-Coelho ◽  
Didier Majou ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Linolenic Acid ◽  
Unsaturated Fatty Acids ◽  
Dietary Lipids ◽  
Alpha Linolenic Acid ◽  
Lipid Fractions ◽  
The Impact ◽  
And Oxidative Stress

Abstract We investigated the impact of increased alpha-linolenic acid (ALA) dietary levels on its plasma bioavailability and its bioconversion in n-3 long chain poly unsaturated fatty acids (LC-PUFA) during a 60-day kinetics and the oxidative stress potentially associated. Rats were submitted to a normolipidic diet providing 0, 3, 10 and 24% ALA of dietary lipids during a kinetics of 0, 15, 30 and 60 days. The lipid peroxidation and oxidative stress (nitric oxide (NO) contents and catalase (CAT), superoxide dismutase (SOD), gluthation peroxidase (GPx) activities) were studied in the liver and plasma. Data demonstrated that when the diet was deprived in n-3 PUFAs, ALA, (eicosanoic acid) EPA and docosahexaenoic acid (DHA) levels decreased in all lipid fractions of plasma and in red blood cell (RBC) lipids. However when ALA was added in the diet, its bioavailability and its bioconversion in EPA was linearly correlated with the ALA intake (R2=0.98). When the diet provided 10 to 24% ALA in dietary lipids (LA/ALA, 1.6 and 5.5 respectively), ALA and EPA were more broadly packaged in all lipid fractions (triglyceride (TG), cholesterol ester (CE) and free fatty acids (FFA)) of plasma from 15 to 30 days timeframe. However only 3% ALA in the lipid diet was sufficient to promote the maximal bioconversion of ALA in DHA in phospholipid (PL) and TG fractions. Additionally, the improvement of ALA bioconversion in EPA and DHA did not impact the oxidative stress markers wich can limit lipid peroxidation. To conclude, this study demonstrated that 10% ALA in the diet for 15-30 days is the gold diet to promote its bioavailability and its bioconversion in n-3 PUFAs in rat and allowed the greatest levels in plasma and RBCs.

scholarly journals Lipid Peroxidation: Aging Kidney

2021 ◽  
Author(s):  
Harnavi Harun
Keyword(s):  
Oxidative Stress ◽  
Reactive Oxygen Species ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Free Radicals ◽  
Reactive Oxygen ◽  
The Elderly ◽  
Nitrogen Species ◽  
Age Related ◽  
Aging Kidney

Kidney is one of the tissues affected by age that involves cellular and structural changes inside the kidney and notably implicates with comorbidity, related to cardiovascular disease aging. Aging kidney causes the elderly susceptible to clinical deterioration from ordinary stimulation that younger individual can compensate, including acute renal injury, volume depletion or overload, sodium and potassium level disorders, and toxic reaction against kidney excreted drugs. As one of the organs with the fastest aging rate, kidney shows several age-related decline in both structural and functional with 30% of the glomerulus are damaged and represent diffuse glomerular sclerosis by age 75 and explain why the prevalence of chronic kidney disease (CKD) and end-stage renal disease are very common in the elderly. The cross-sectional population-based study by The National Health and Nutrition Examination Survey supports the theory of age-related decline in kidney function, although some other subjects did not have an absolute decline in kidney function. The underlying molecular mechanisms could be the target of future therapeutic strategies. Aging is a natural biological process characterized by a gradual decline in cellular function as well as progressive structural change of organ systems. In aging kidney, there are interactions of genetic factors, environmental changes, and cellular dysfunction that lead to the typical structural and functional changes. One of the most popular theory of aging is the theory of free radicals or oxidative stress based on the fact that cells are under chronic oxidative stress due to an imbalance between pro oxidants and antioxidants. Reactive oxygen species are oxygen-derived oxidizing compounds that are highly reactive, consisting of free radicals and non-radicals. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) refer to both reactive radicals and non-radical derivatives of oxygen and nitrogen. Reactive oxygen and nitrogen species (RONS) are produced by all aerobic cells and play an important role in aging as well as age-related diseases. Lipid peroxidation is a process of oxidative degradation of lipids that process by which free radicals bind to lipid electrons in the cell membrane resulting in direct cell damage. Lipid peroxidation can cause cellular damage in several ways such as impairing the integrity of the plasma membrane and subcellular organelles by peroxidation, “chain reaction” of ROS production, and activation of phospholipase A2 (PLA2) caused by lipid peroxidation. Fatty acids and other PLA2 metabolites (such as lysophospholipids) are known to damage cell membranes. In the development of kidney damage, the process of lipid peroxidation plays an important role. This is presumably due to the large number of long-chain polyunsaturated fatty acids (PUFAs) in the lipid composition of the kidneys and there are substantial evidence to suggest that ROS is involved in the ischemic, toxic, and immunologically mediated pathogenesis of renal injury, but the cellular mechanisms that result in cell injury and death are still being studied.

scholarly journals Protective Effect of Natural and Synthetic Anthocyanins against Tert-butyl-hydroperoxide-induced Oxidative Damages in Normal and β-thalassemic Major Human Erythrocytes In Vitro

2020 ◽  
Vol 17 (1) ◽  
pp. 38-47
Author(s):  
Naïma Charif ◽  
Nassima Mokhtari-Soulimane ◽  
Sabri Cherrak ◽  
Hafida Merzouk ◽  
Mourad Elhabiri
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Thalassemia Major ◽  
Dpph Assay ◽  
Butyl Hydroperoxide ◽  
Tert Butyl ◽  
Oxidative Damages ◽  
Blood Disorder ◽  
Tert Butyl Hydroperoxide

Background: Even though β-thalassemia major is a genetic blood disorder, the damages endured by erythrocytes are mediated in part by oxidative stress. Antioxidants such as anthocyanins are capable to prevent the pro-oxidant effects induced by reactive oxygen species (ROS). Objective: This study aims to evaluate the in vitro preventive effects of one natural and two synthetic anthocyanins on normal and β-thalassemic erythrocytes on which toxicity has been induced by the free radical generator: tert-butyl-hydroperoxide TBHP. Methods: Erythrocytes isolated from fasting blood samples of healthy and β-thalassemic major individuals were treated either with TBHP alone or with TBHP after being pre-incubated with anthocyanins. Cell viability, reduced glutathione (GSH) and malondialdehyde (MDA) contents were measured after 90 minutes of incubation. In parallel, the antiradical scavenging capacities of the investigated anthocyanins were also estimated by using the 2,2-DiPhenyl-1-PicrylHydrazyl (DPPH•) assay. Results: The results clearly demonstrate that the treatment of erythrocytes with TBHP induces hemolysis along with marked redox state alteration (lipid peroxidation concomitant to GSH depletion) in both normal and β-thalassemia erythrocytes. During the pre-treatment with anthocyanins, erythrocytes become more resistant to oxidative impairments. Cyanin chloride and 6,7,3’,4’- tetrahydroxyflavylium chloride effectively prevent from TBHP-induced: hemolysis, lipid peroxidation and GSH depletion in normal and thalassemic erythrocytes, while 3’4’-dihdroxy-7-methoxyflavylium chloride had a lesser effect on MDA levels with thalassemic erythrocytes. These results are in agreement with those derived from the DPPH• assay. Conclusion: Our study contributes with important insights that tested anthocyanins may exert relevant potential in the alleviation of oxidative stress, especially the one affecting β-thalassemia erythrocytes.

scholarly journals Effects of a Fish Oil Rich in Docosahexaenoic Acid on Cardiometabolic Risk Factors and Oxidative Stress in Healthy Rats

Marine Drugs ◽  
2021 ◽  
Vol 19 (10) ◽  
pp. 555
Author(s):  
Bernat Miralles-Pérez ◽  
Lucía Méndez ◽  
Maria Rosa Nogués ◽  
Vanessa Sánchez-Martos ◽  
Àngels Fortuño-Mar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Risk Factors ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Docosahexaenoic Acid ◽  
Fish Oil ◽  
Soybean Oil ◽  
Cardiometabolic Risk ◽  
Coconut Oil ◽  
And Oxidative Stress

Omega-3 polyunsaturated fatty acids are associated with a lower risk of cardiometabolic diseases. However, docosahexaenoic acid (DHA) is easily oxidized, leading to cellular damage. The present study examined the effects of an increased concentration of DHA in fish oil (80% of total fatty acids) on cardiometabolic risk factors and oxidative stress compared to coconut oil, soybean oil, and fish oil containing eicosapentaenoic acid (EPA) and DHA in a balanced ratio. Forty healthy male Sprague–Dawley rats were supplemented with corresponding oil for 10 weeks. Supplementation with the fish oil containing 80% DHA decreased plasma fat, plasma total cholesterol and muscle fat compared to the coconut oil and the soybean oil. Increasing concentrations of DHA induced incorporation of DHA and EPA in cell membranes and tissues along with a decrease in ω-6 arachidonic acid. The increase in DHA promoted lipid peroxidation, protein carbonylation and antioxidant response. Taken together, the increased concentration of DHA in fish oil reduced fat accumulation compared to the coconut oil and the soybean oil. This benefit was accompanied by high lipid peroxidation and subsequent protein carbonylation in plasma and in liver. In our healthy framework, the slightly higher carbonylation found after receiving fish oil containing 80% DHA might be a protecting mechanism, which fit with the general improvement of antioxidant defense observed in those rats.

scholarly journals Induction of Mitochondrial Changes Associated with Oxidative Stress on Very Long Chain Fatty Acids (C22:0, C24:0, or C26:0)-Treated Human Neuronal Cells (SK-NB-E)

2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Amira Zarrouk ◽  
Anne Vejux ◽  
Thomas Nury ◽  
Hammam I. El Hajj ◽  
Madouda Haddad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Fatty Acids ◽  
Cell Counting ◽  
Long Chain Fatty Acids ◽  
Superoxide Anion Production ◽  
Mitochondrial Dysfunctions ◽  
Whole Cells ◽  
Potential Risk Factors ◽  
Long Chain ◽  
Chain Fatty Acids

In Alzheimer's disease, lipid alterations point towards peroxisomal dysfunctions. Indeed, a cortical accumulation of saturated very long chain fatty acids (VLCFAs: C22:0, C24:0, C26:0), substrates for peroxisomalβ-oxidation, has been found in Alzheimer patients. This study was realized to investigate the effects of VLCFAs at the mitochondrial level since mitochondrial dysfunctions play crucial roles in neurodegeneration. On human neuronal SK-NB-E cells treated with C22:0, C24:0, or C26:0 (0.1–20 μM; 48 h), an inhibition of cell growth and mitochondrial dysfunctions were observed by cell counting with trypan blue, MTT assay, and measurement of mitochondrial transmembrane potential (Δψm) with DiOC6(3). A stimulation of oxidative stress was observed with DHE and MitoSOX used to quantify superoxide anion production on whole cells and at the mitochondrial level, respectively. With C24:0 and C26:0, by Western blotting, lower levels of mitochondrial complexes III and IV were detected. After staining with MitoTracker and by transmission electron microscopy used to study mitochondrial topography, mass and morphology, major changes were detected in VLCFAs treated-cells: modification of the cytoplasmic distribution of mitochondria, presence of large mitochondria, enhancement of the mitochondrial mass. Thus, VLCFAs can be potential risk factors contributing to neurodegeneration by inducing neuronal damages via mitochondrial dysfunctions.

scholarly journals Phytotherapeutics Attenuation of Oxidative Stress, Inflammation and Lipid Peroxidation in Severe and Chronic Diseases

2021 ◽  
Author(s):  
Mavondo-Nyajena Mukuwa Greanious Alfred ◽  
Ncube Nesisa ◽  
Sibanda Alfred ◽  
Dube Delton ◽  
Chikuse Francis Farai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Current Treatment ◽  
Natural Food ◽  
Reaction Cell ◽  
Signaling Systems ◽  
Treatment Regimens ◽  
Disease States

Lipid peroxidation is an end process of cellular injury driven by oxidative stress (OS) and inflammation through several molecular changes. Metabolism-generated reactive oxygen species avidly attack the polyunsaturated fatty acids in lipid cell membranes, initiating a self-propagating chain-reaction. Cell membrane destruction, lipids and the end-products of lipid peroxidation reactions are hostile to the viability of cells, even tissues causing and exacerbating Diabetes Mellitus (DM), neurodegenerative disorders (NDDs), cardiovascular diseases (CVDs) and Rheumatoid Arthritis (RA). Current treatment regimens have untoward side effects in the long-term necessitating phytochemical use as these are part of natural food sources. Enzymatic and non-enzymatic antioxidant defense mechanisms may be over run causing lipid peroxidation to take place. In disease states, oxidative stress may increase with subsequent production of increased free radicals which may over run the antioxidant capacity of the body with resultant oxidative damage on polyunsaturated fatty acids in the cell fluid membranes with cellular and tissue damage. Phytochemicals, have been shown to ameliorate diseases through attenuation of oxidative stress, inflammation, lipid peroxidation, causing tissue regeneration by regulating signaling systems and neuroprotective processes. Involvement of polyphenolic and non-phenolic phytochemical in the attenuation of OS, inflammation and lipid peroxidation remain areas of critical importance in combating DM, CVDA, NDD and RA.

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