What is not the problem:
Linoleic acid is an omega 6 essential fatty acid. Consumption of unoxidized linoleic acid as found in raw, organic seeds is vital to human survival. Unoxidized linoleic acid, even when consumed in excess, does not form arachidonic acid as was hypothesized that linoleic acid formed arachidonic ,and linked to inflammation. Even though this hypothesis has been shown to be scientifically inaccurate by meta analysis, the misunderstanding has continued. In our consortium’s research involving examination of red cell fatty acids for the past 25 years at a university-based laboratory, we have observed that in prolonged vegetarianism that the body will convert linoleic acid into arachidonic acid as an act of survival. Alpha Linolenic acid, an omega 3 essential fatty acid, is also prevalent in seed oils and is even more vulnerable to oxidation as it is more unsaturated than linoleic acid.
*Consumption of unoxidized alpha linolenic acid as found in raw, organic seeds/ walnuts is also vital to human health, and serves as a ‘lipid whisker’ attached to the phospholipids in cell membranes. There is a balance to parent essential fatty acids that Shlomo Yehuda developed with 4 parts of linoleic acid to 1 part of alpha linolenic acid called the SR3 ratio.
MANY INDUSTRIAL OILS ARE NOW HYBRIDS, HIGH OLEIC, NOT HIGH LINOLEIC:
Once the scientific literature exposed that partially hydrogenated oils were a serious health risk, industry introduced hybrid seeds with high oleic acid content so that heat extraction and shelf life could be extended with commercial foods. Approximately 10 years ago commercial oils were introduced made from hybrid high OLEIC ACID rather than the natural high linoleic content. Check the ingredients on food labels, even natural food, it states ‘high oleic soy oil’, high oleic corn oil’, high oleic sunflower oil’, etc.
DIFFICULTY OF ASSESSING THE LITERATURE DUE TO THE PREVALENCE OF TRANS FAT :
Scouring the scientific literature for verification of the risks industrialized oils cause is difficult as partially hydrogenated oils were the prevalent source of oil in the American
food supply. Thus, dated population studies are not supportive to the negative effects of lipid oxidation as trans fats have been determined to be harmful. Once commercial oils are purchased they are often heated further in cooking, most problematic with frying. The use of industrialized oils used in fast food chains causes further breakdown of the triglycerides, releasing free fatty acids leading to further oxidation of the oil and the formation of toxic compounds, free radicals, from thermal decomposition, resulting in high levels of reactive oxygen species (ROS) defined as unpaired electrons that are unstable and highly reactive.
WHY DO COMMERCIAL, INDUSTRIAL OILS PRESENT HEALTH RISKS :
The medical literature does not give us substantiation as to why industrial oils are harmful to the body, as it was never a focus of inquiry. However, there is medical literature that hypothesizes that omega 6, specifically linoleic acid, is harmful, overconsumed and the cause of American health challenges. One cannot equate a source of oxidized (damaged) linoleic acid obtained from industrialized seed oil manufacturing to unoxidized linoleic acid from whole, raw seeds or supercritical CO2 extraction of oil obtained from seeds. Lipid researchers find it preposterous to suggest that linoleic acid, an essential fatty acid, is harmful, or that it should be limited. To clarify, its about the balance of linoleic to alpha linolenic. Some individuals have gone so far as to say, in error, that the consumption of seeds should be limited. We do know, however, from the medical literature that overdosing with enormous amounts of linoleic acid does not in any way evoke inflammation, but there is concern if a source of alpha linolenic is missing from the diet along with a source of fish. This is due to the fact the same enzyme that converts linoleic acid into gamma linolenic acid (GLA) competes for the same enzyme that converts alpha linolenic acid into EPA. It is crucial to balance the parent oils linoleic and alpha linoleic, but also of note they have in their own right enormous function within the cell. Thus, there would be a negative effect if enormous amounts of linoleic acid was consumed with limited access to alpha linolenic acid in the diet (seeds do contain both linoleic and alpha linolenic), and no fish was consumed to supply EPA and DHA. The conversion from alpha linolenic acid to EPA is severely limited, perhaps 1% conversion, thus fish or caviar needs to be consumed.
When polyunsaturated fatty acids, such as linoleic acid or alpha linolenic acid (both found in seed oils and both vulnerable to oxidation) are heated to high temperatures by extraction processes, and often further exposed to high temperatures as in fried food, especially in restaurants where the oil is repeatedly reused, there is a serious health risk due to:
Overall, polyunsaturated oils simply should not be heated, or used for cooking as they oxidize. The extraction process must minimize heat. Even oleic acid, which is monounsaturated, is oxidized when exposed to high heat. Immediate attention must be given to oils used in food service as frying oil is reused for months accelerating oxidation and formation of toxic compounds that are absorbed into food. There are no oil quality oxidation regulations in the United States, however, there are in other countries.
Aberrant fatty acids in commercial oil sources
Canola oil and peanut oil, apart from being industrialized oils, contain very long chain fatty acids (VLCFAs) that form debris inside the cell, which can impair liver and brain metabolism due to necessary upregulation of peroxisomal respiration to dispose of them through beta oxidization. Canola oil also contains alpha linolenic acid, which is more unsaturated than linoleic, more vulnerable to oxidation.
Chemicals solvents are also used for industrial oil extraction such as hexane (heptanes, cyclohexan, methyloxolane, acetone) and pose serious health risks, especially to the neurological system. The danger of hexane came to light when it was used to extract
omega 3 DHA from blue green micro-algae and added to baby formula.
There is no regulatory limit from the FDA on residual hexane in industrial oils
It is estimated that residual hexane is ‘typically less than 1 PPM’ but no testing is required.
Green solvents, plant-based terpenes, are a consideration to replace toxic solvents.
Ethanol extraction of oils preserves the polyphenols naturally within the oil, but the oil then contains ethanol
The antioxidant Alpha tocopherol naturally contained in oil is protective against oxidation giving it stability, but when oil is heated the alpha tocopherol is the first to be oxidized and as that level drops, the oil readily oxidizes, even if other forms of tocopherols (delta, gamma) are still present. Some have suggested adding additional alpha tocopherol to stabilize refined oil.
Pesticide residue is substantial in seed oils, which the refining of oil removes to some extent. It is suggested by the industry to only use organic oils as the raw material if a cold pressed extraction method is used.
High Oleic Commercial Oils are now predominant in the US food supply
Hybrid seeds with a high oleic content were introduced ~ 10 years ago to prolong shelf life and lower potential for rancidity as the unsaturated fatty acid linoleic acid was lowered.
Alternative Extraction and Refining Methods
Supercritical CO2 extraction of oils is the best option to prevent polyunsaturated oils from becoming oxidized. This extraction method is expensive, but the best method highly unsaturated fatty acids (HUFA) like GLA, EPA and DHA should be extracted.
Tallow, which is derived from suet, is the solid fat surrounding the organs of a cow (or sheep, goat) contains ~ 43% saturated fat and ~ 50% monounsaturated fatty acids (oleic), and cholesterol. Both oleic acid and cholesterol can oxidize at high temperatures. If the tallow is repeatedly heated there is an increase in free fatty acids and oxidation of the monounsaturates. Tallow is lower in arachidonic acid than lard, averaging 100 mg per 100 grams of fat (dependent upon what the animal has consumed). Toxins accumulate in the fat of animals. Tallow is inexpensive.
Lard contains saturated fatty acids (palmitic and stearic) at 37%, along with oleic acid at
~ 46%, and ~ 17% polyunsaturated fatty acids (PUFA) depending on what the animal consumed. Lard contains 1700 mg of arachidonic acid per 100 grams. Lard contains more oleic acid than butter. Toxins accumulate in the fat of animals. Lard is inexpensive.
Palm oil contains palmitic acid, a saturated fatty acid, which DOES lead to inflammation as palmitic acid* induces a macrophage inflammatory response through activation of toll-like receptors involved in the innate immune response. Sourcing of palm oil is limited, thus cannot replace industrial seed oils. The overconsumption of palmitic acid and consequent elevation in red cells can be suppressed by competitive inhibition with Linoleic acid.
Coconut oil contains saturated fatty acids Lauric (45-56%), Myristic (16-21%), Palmitic (7.5-10.2%), small amounts of Caprylic and Capric acids. Coconut has a higher smoke point than mono or polyunsaturated fatty acids, thus is a safer alternative for cooking.
There is limited availability of coconut oil, it is expensive, but less expensive than olive oil.
*MCT oil contains caprylic (C8:0), capric (C10:0), Lauric (C12:0) and is used for therapeutic medical diets, and by health enthusiasts, and is very expensive.
Extra virgin olive oil contains 80% oleic acid, with palmitic and stearic fatty acids.. Olive oil contains potent polyphenols, which has a protective effect against oxidation during the cooking process. However, the monounsaturate within olive oil, oleic acid, can oxidize when exposed to heat. The taste of olive oil limits its addition to some foods. Extra Virgin Olive oil is expensive
at $50+ per gallon.
Extra virgin avocado oil contains primarily palmitic acid, but also stearic and oleic acid. The smoke point of avocado oil is higher than that of olive oil. Avocado oil has a lower level of polyphenols and is more expensive than olive oil.
Ghee /Clarified butter contains primarily palmitic, with stearic, myristic, lauric, butyric
Arachidonic acid content ~ 110 mg per 100 grams. Higher smoke point than butter.
*Saturated fatty acids (Palmitic, Stearic) are biosynthesized in the body, thus are not essential.
Assessing the result of ultra processed food upon the health and development of children
Industrial, processed oils are one of many ingredients within ultra-processed foods. Processed food represents empty calories, synthetic additives, chemical residues, pesticides and fungus are part of the equation of ultra processed food along with
industrial oils. Exposure to toxins causes oxidation in the body, thus it is difficult to separate the effect toxins have had on the polyunsaturates in cells opposed to the consumption of industrialized oils, which is often consumed with further exposure to heat as fried food. Ultra-processed food lacks nutrient density, and if food in its natural form is lacking in the diet, nutritional requirements will not be met. Children on an ultra-processed food diet may experience failure to thrive, a delay in linear growth, and not reach their potential, which may result in intellectual deficits and emotional instability .
What is the Essential Fatty Acid Intake ?
Another important consideration is not just what is being consumed that has a potentially negative effect upon the body, but what is NOT being consumed. Natural whole foods that contain essential fatty acids have been altered in food processing as well as cooking methods that further degrade nutrient availability. The introduction of hybrid high oleic oils that can be observed on both natural food products and commercial products state:
High Oleic Safflower oil, High Oleic Soy oil, High Oleic Sunflower oil, High Oleic Corn oil
on the label thus the level of linoleic acid is much reduced and no longer in the equation as it was 10 years ago prior to the introduction of hybrid oils.
Examination of red cell fatty acids and phospholipids from university-based laboratories give a systemic view of the abnormalities caused by inadequate dietary intake, consumption of industrialized oils, potential aberrant lipids both consumed, biosynthesized due to epigenetic insult and/or impaired peroxisomal respiration as oxidized phospholipids and very long chain/odd chain and branched chain fatty acids.
Malondialdehyde, a degradation product of lipid peroxides, can be measured in the blood as can thiobarbituric reactive substances (TBARS) for lipid peroxidation products, cholesterol oxidized products of oxidation such as isoprostanes, lipid hydroperoxides and oxyserols, but these tests do not identify the source of the lipid peroxidation in the body as theses markers in the blood may be caused by toxic insult.
Imaging of cells can reveal oxidized lipids attached to the cell membrane and cellular components, including as DNA adducts in epigenetic test sets and imaging studies on blood and tissue samples.
Damage to the GI tract can occur with the consumption of industrialized oils, and fried food whereby the oil used is highly oxidized. Oxidation products consumed as in industrialized oils and/or in food after further cooked at high temperatures, i.e. French fries, have the potential to cause damage to the intestinal lining and markedly disrupt the microbiome as described in a 2017 paper by Vierira, Zhang and Decker. In 2025 Wang et al found that oxidized linoleic acid, but not unoxidized linoleic acid promoted colitis and colitis-associated tumorigenesis in a mouse model.
References
Journal of the American Oil Chemists Society, Vol 94, pages 339-351, 2017
Biological Implications of Lipid Oxidation Products
Vieira SA, Zhang G, Decker EA
Abstract
Essentially all fat-containing foods have the potential to undergo lipid oxidation even where unsaturated fatty acid compositions are low. Therefore, consumption of lipid oxidation products is potentially common with risk of consuming lipid oxidation products increasing in foods with high amounts of unsaturation (e.g. foods with omega-3 fatty acids), foods subjected to extensive thermal processing (e.g. fried foods), or food high in pro-oxidants (e.g. meats). Lipid oxidation generates potentially toxic products that have shown correlation with inflammatory diseases, as well as cancer, atherosclerosis, aging, etc. These potentially toxic products can enter the body through the diet and can develop in vivo during the digestion of lipids. Oxidation products can be absorbed into the blood and in some cases transported to tissues. The aim of this manuscript is to review how potentially toxic lipid oxidation products are formed and evaluate their potential to impact health. While lipid oxidation produces literally hundreds of oxidation products, this review focused on acrolein, 4-hydroxy-trans-nonenal, 4-hydroxy-trans-hexanal, crotonaldehyde, malondialdehyde, and cholesterol as they are the most reactive oxidation products and also the most studied.
J Crohns Colitis 2025 Mar 5;19(3):jjae148.
Oxidized Polyunsaturated Fatty Acid Promotes Colitis and Colitis-Associated Tumorigenesis in Mice
Weicang Wang 1 2, Yuxin Wang 1 2, Katherine Z Sanidad 1 3 4 5, Yige Wang 6, Jianan Zhang 1, Wenqi Yang 6, Quancai Sun 7, Ipek Bayram 1, Renhua Song 8 9, Haixia Yang 1, David Johnson 1, Heather L Sherman 10, Daeyoung Kim 11, Lisa M Minter 3 10, Justin J-L Wong 8 9, Melody Y Zeng 4 5, Eric A Decker 1, Guodong Zhang 1 6
PMID: 39279209 DOI: 10.1093/ecco-jcc/jjae148
Abstract
Background and aims: Human studies suggest that a high intake of polyunsaturated fatty acid (PUFA) is associated with an increased risk of inflammatory bowel disease (IBD). PUFA is highly prone to oxidation. To date, it is unclear whether unoxidized or oxidized PUFA is involved in the development of IBD. Here, we aim to compare the effects of unoxidized PUFA vs oxidized PUFA on the development of IBD and associated colorectal cancer.
Methods: We evaluated the effects of unoxidized and oxidized PUFA on dextran sodium sulfate (DSS)-induced and IL-10 knockout-induced colitis, and azoxymethane/DSS-induced colon tumorigenesis in mice. Additionally, we studied the roles of gut microbiota and Toll-like receptor 4 (TLR4) signaling involved.
Results: Administration of a diet containing oxidized PUFA, at human consumption-relevant levels, increases the severity of colitis and exacerbates the development of colitis-associated colon tumorigenesis in mice. Conversely, a diet rich in unoxidized PUFA does not promote colitis. Furthermore, oxidized PUFA worsens colitis-associated intestinal barrier dysfunction and leads to increased bacterial translocation, and it fails to promote colitis in TLR4 knockout mice. Finally, oxidized PUFA alters the diversity and composition of gut microbiota, and it fails to promote colitis in mice lacking the microbiota.
Conclusions: These results support that oxidized PUFA promotes the development of colitis and associated tumorigenesis in mouse models via TLR4- and gut microbiota-dependent mechanisms. Our findings highlight the potential need to update regulation policies and industrial standards for oxidized PUFA levels in food.
Keywords: Polyunsaturated fatty acid; colitis; colitis-associated tumorigenesis; lipid oxidation.
Nutrients. 2018 May 24;10(6):668. doi: 10.3390/nu10060668.
The Eye, Oxidative Damage and Polyunsaturated Fatty Acids.
Saccà SC, Cutolo CA, Ferrari D, Corazza P, Traverso CE.
PMID: 29795004 Free PMC article. Review.
Abstract
Ferroptosis is form of regulated nonapoptotic cell death that is involved in diverse disease contexts. Small molecules that inhibit glutathione peroxidase 4 (GPX4), a phospholipid peroxidase, cause lethal accumulation of lipid peroxides and induce ferroptotic cell death. Although ferroptosis has been suggested to involve accumulation of reactive oxygen species (ROS) in lipid environments, the mediators and substrates of ROS generation and the pharmacological mechanism of GPX4 inhibition that generates ROS in lipid environments are unknown. We report here the mechanism of lipid peroxidation during ferroptosis, which involves phosphorylase kinase G2 (PHKG2) regulation of iron availability to lipoxygenase enzymes, which in turn drive ferroptosis through peroxidation of polyunsaturated fatty acids (PUFAs) at the bis-allylic position; indeed, pretreating cells with PUFAs containing the heavy hydrogen isotope deuterium at the site of peroxidation (D-PUFA) prevented PUFA oxidation and blocked ferroptosis. We further found that ferroptosis inducers inhibit GPX4 by covalently targeting the active site selenocysteine, leading to accumulation of PUFA hydroperoxides. In summary, we found that PUFA oxidation by lipoxygenases via a PHKG2-dependent iron pool is necessary for ferroptosis and that the covalent inhibition of the catalytic selenocysteine in Gpx4 prevents elimination of PUFA hydroperoxides; these findings suggest new strategies for controlling ferroptosis in diverse contexts.
Keywords: Gpx4; PHKG2; PUFAs; ferroptosis; lipoxygenase.
Review Biochem Biophys Res Commun. 2017 Jan 15;482(3):419-425. doi: 10.1016/j.bbrc.2016.10.086. Epub 2017 Feb 3.
Lipid peroxidation in cell death
Michael M Gaschler 1, Brent R Stockwell 2
PMID: 28212725 PMCID: PMC5319403 DOI: 10.1016/j.bbrc.2016.10.086
Abstract
Disruption of redox homeostasis is a key phenotype of many pathological conditions. Though multiple oxidizing compounds such as hydrogen peroxide are widely recognized as mediators and inducers of oxidative stress, increasingly, attention is focused on the role of lipid hydroperoxides as critical mediators of death and disease. As the main component of cellular membranes, lipids have an indispensible role in maintaining the structural integrity of cells. Excessive oxidation of lipids alters the physical properties of cellular membranes and can cause covalent modification of proteins and nucleic acids. This review discusses the synthesis, toxicity, degradation, and detection of lipid peroxides in biological systems. Additionally, the role of lipid peroxidation is highlighted in cell death and disease, and strategies to control the accumulation of lipid peroxides are discussed
Int J Med Sci. 2021 Jul 25;18(15):3361-3366. doi: 10.7150/ijms.62903. eCollection 2021.
Ferroptosis and Liver Fibrosis.
Pan Q, Luo Y, Xia Q, He K.
PMID: 34522161 Free PMC article. Review.
Abstract
Ferroptosis is form of regulated nonapoptotic cell death that is involved in diverse disease contexts. Small molecules that inhibit glutathione peroxidase 4 (GPX4), a phospholipid peroxidase, cause lethal accumulation of lipid peroxides and induce ferroptotic cell death. Although ferroptosis has been suggested to involve accumulation of reactive oxygen species (ROS) in lipid environments, the mediators and substrates of ROS generation and the pharmacological mechanism of GPX4 inhibition that generates ROS in lipid environments are unknown. We report here the mechanism of lipid peroxidation during ferroptosis, which involves phosphorylase kinase G2 (PHKG2) regulation of iron availability to lipoxygenase enzymes, which in turn drive ferroptosis through peroxidation of polyunsaturated fatty acids (PUFAs) at the bis-allylic position; indeed, pretreating cells with PUFAs containing the heavy hydrogen isotope deuterium at the site of peroxidation (D-PUFA) prevented PUFA oxidation and blocked ferroptosis. We further found that ferroptosis inducers inhibit GPX4 by covalently targeting the active site selenocysteine, leading to accumulation of PUFA hydroperoxides. In summary, we found that PUFA oxidation by lipoxygenases via a PHKG2-dependent iron pool is necessary for ferroptosis and that the covalent inhibition of the catalytic selenocysteine in Gpx4 prevents elimination of PUFA hydroperoxides; these findings suggest new strategies for controlling ferroptosis in diverse contexts.
Keywords: Gpx4; PHKG2; PUFAs; ferroptosis; lipoxygenase.
Review Biochem Biophys Res Commun. 2005 Dec 9;338(1):668-76. doi: 10.1016/j.bbrc.2005.08.072. Epub 2005 Aug 19.
Lipid peroxidation: mechanisms, inhibition, and biological effects
Etsuo Niki 1, Yasukazu Yoshida, Yoshiro Saito, Noriko Noguchi
Affiliations Expand
PMID: 16126168 DOI: 10.1016/j.bbrc.2005.08.072
Abstract
In the last 50 years, lipid peroxidation has been the subject of extensive studies from the viewpoints of mechanisms, dynamics, product analysis, involvement in diseases, inhibition, and biological signaling. Lipids are oxidized by three distinct mechanisms; enzymatic oxidation, non-enzymatic, free radical-mediated oxidation, and non-enzymatic, non-radical oxidation. Each oxidation mechanism yields specific products. The oxidation of linoleates and cholesterol is discussed in some detail. The relative susceptibilities of lipids to oxidation depend on the reaction milieu as well as their inherent structure. Lipid hydroperoxides are formed as the major primary products, however they are substrates for various enzymes and they also undergo various secondary reactions. Phospholipid hydroperoxides, for example, are reduced to the corresponding hydroxides by selenoproteins in vivo. Various kinds of antioxidants with different functions inhibit lipid peroxidation and the deleterious effects caused by the lipid peroxidation products. Furthermore, the biological role of lipid peroxidation products has recently received a great deal of attention, but its physiological significance must be demonstrated in future studies.
Review Biochem Biophys Res Commun. 2017 Jan 15;482(3):419-425. doi: 10.1016/j.bbrc.2016.10.086. Epub 2017 Feb 3.
Lipid peroxidation in cell death
Michael M Gaschler 1, Brent R Stockwell 2
Affiliations Expand
PMID: 28212725 PMCID: PMC5319403 DOI: 10.1016/j.bbrc.2016.10.086
Abstract
Disruption of redox homeostasis is a key phenotype of many pathological conditions. Though multiple oxidizing compounds such as hydrogen peroxide are widely recognized as mediators and inducers of oxidative stress, increasingly, attention is focused on the role of lipid hydroperoxides as critical mediators of death and disease. As the main component of cellular membranes, lipids have an indispensible role in maintaining the structural integrity of cells. Excessive oxidation of lipids alters the physical properties of cellular membranes and can cause covalent modification of proteins and nucleic acids. This review discusses the synthesis, toxicity, degradation, and detection of lipid peroxides in biological systems. Additionally, the role of lipid peroxidation is highlighted in cell death and disease, and strategies to control the accumulation of lipid peroxides are discussed.
Keywords: Antioxidant; Ferroptosis; Lipid oxidation; Neurodegeneration; Oxidation; Peroxidation.
Oxid Med Cell Longev. 2019 Nov 27;2019:7147235. doi: 10.1155/2019/7147235
Lipid Peroxidation Products in Human Health and Disease 2019
Kota V Ramana 1,✉, Sanjay Srivastava 2, Sharad S Singhal 3
PMCID: PMC6900947 PMID: 31885812
Oxidative stress is the major cause of several life-threatening complications including various forms of cancers. Exposure of the body to external pathogens, xenobiotics, allergens, and environmental pollutants leads to increased generation of reactive oxygen species (ROS). The ROS thus generated can interact with important cellular molecules causing the disturbance in the cellular redox balance leading to various pathological consequences. One of the most important molecules directly affected by ROS is polyunsaturated fatty acids. ROS-mediated peroxidation of lipids forms various toxic lipid hydroperoxides and lipid aldehydes which act as secondary signaling intermediates in propagating the oxidative stress signals which contribute to the pathophysiology of human health and disease. Recent studies have demonstrated that the lipid peroxidation-derived lipid aldehydes regulate a number of human pathological complications including cancer, diabetes, cardiovascular, neurological, and various inflammatory diseases. Recent evidence also suggests that lipid peroxidation-derived lipid aldehydes act as biomarkers of various disease processes such as Alzheimer's and Parkinson's. Thus, continuous research work on lipid peroxidation and its generated products is very important in identifying the novel signaling mechanisms involved various human diseases and to explore possible biomarkers of disease and develop better therapeutic approaches. Through a series of special issues, we are continuously encouraging investigators to share their novel research work highlighting the significance of lipid peroxidation products in the pathophysiology of various human diseases.
Antioxidants (Basel). 2022 Oct 20;11(10):2071. doi: 10.3390/antiox11102071.
Detrimental Effects of Lipid Peroxidation in Type 2 Diabetes: Exploring the Neutralizing Influence of Antioxidants
Samukelisiwe C Shabalala 1 2, Rabia Johnson 1 3, Albertus K Basson 2, Khanyisani Ziqubu 4, Nokulunga Hlengwa 2, Sinenhlanhla X H Mthembu 1 4, Sihle E Mabhida 1, Sithandiwe E Mazibuko-Mbeje 4, Sidney Hanser 5, Ilenia Cirilli 6, Luca Tiano 6, Phiwayinkosi V Dludla 1 2
PMID: 36290794 PMCID: PMC9598619 DOI: 10.3390/antiox11102071
Abstract
Lipid peroxidation, including its prominent byproducts such as malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE), has long been linked with worsened metabolic health in patients with type 2 diabetes (T2D). In fact, patients with T2D already display increased levels of lipids in circulation, including low-density lipoprotein-cholesterol and triglycerides, which are easily attacked by reactive oxygen molecules to give rise to lipid peroxidation. This process severely depletes intracellular antioxidants to cause excess generation of oxidative stress. This consequence mainly drives poor glycemic control and metabolic complications that are implicated in the development of cardiovascular disease. The current review explores the pathological relevance of elevated lipid peroxidation products in T2D, especially highlighting their potential role as biomarkers and therapeutic targets in disease severity. In addition, we briefly explain the implication of some prominent antioxidant enzymes/factors involved in the blockade of lipid peroxidation, including termination reactions that involve the effect of antioxidants, such as catalase, coenzyme Q10, glutathione peroxidase, and superoxide dismutase, as well as vitamins C and E.Keywords: antioxidants; inflammation; lipid peroxidation; metabolic complications; oxidative stress; type 2 diabetes.
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