Mavondo-Nyajena Mukuwa Greanious Alfred, Ncube Nesisa, Sibanda Alfred, Dube Delton, Chikuse Francis Farai, Makoni Paul
{"title":"Phytotherapeutics Attenuation of Oxidative Stress, Inflammation and Lipid Peroxidation in Severe and Chronic Diseases","authors":"Mavondo-Nyajena Mukuwa Greanious Alfred, Ncube Nesisa, Sibanda Alfred, Dube Delton, Chikuse Francis Farai, Makoni Paul","doi":"10.5772/intechopen.99832","DOIUrl":"https://doi.org/10.5772/intechopen.99832","url":null,"abstract":"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.","PeriodicalId":426818,"journal":{"name":"Lipid Peroxidation [Working Title]","volume":"1995 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-09-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"131552593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lipid Peroxidation: A Signaling Mechanism in Diagnosis of Diseases","authors":"K. Patil, R. Wadekar","doi":"10.5772/intechopen.99706","DOIUrl":"https://doi.org/10.5772/intechopen.99706","url":null,"abstract":"Quantification of reactive oxygen species, is perplexing either in vivo or in vitro due to their short half-lives. Consequently, to define the magnitude of oxidative stress, the more stable oxidation products can be measured in biological samples. The oxidative stress leads to the lipid peroxidation that involves the initiation, termination and propagation of lipid radicals, wherein, the process involves the oxygen uptake, rearrangement of the double bonds in unsaturated lipids, that leads to polyunsaturated fatty acid deterioration. Subsequently, the toxic signaling end products are considered as biomarkers of free radicals that act both as signaling molecules and as cytotoxic products cause covalent alteration of lipid peroxidation products. The use of validated signaling mechanism (s) of Lipid peroxidation and products derived thereof exhibits its use clinical practice and basic clinical research as well as in clinical practice has become common place, and their presence as endpoints in clinical trials is now broadly accepted. This knowledge can be used to diagnose disease earlier, or to prevent it before it starts. The signaling markers can be used to excel the effectiveness of the prevailing medicines and to improve the new medicines.","PeriodicalId":426818,"journal":{"name":"Lipid Peroxidation [Working Title]","volume":"68 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-08-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"133201243","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
A. Kükürt, V. Gelen, Ömer Başer, H. Deveci, M. Karapehlivan
{"title":"Thiols: Role in Oxidative Stress-Related Disorders","authors":"A. Kükürt, V. Gelen, Ömer Başer, H. Deveci, M. Karapehlivan","doi":"10.5772/INTECHOPEN.96682","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.96682","url":null,"abstract":"The effects of oxidative stress occur as a result of peroxidative damage of the macromolecule and membranes of the cells and with the disruption of metabolic activities in the components of the cells in living organisms. Organ and tissue pathologies are known to occur when oxidative stress is excessive in the body. It is known that thiols are one of the main protective mechanisms of the body against oxidative stress. Thiols have been shown to play important roles in enzymatic reactions, apoptosis, detoxification and antioxidant protection in the body. Many studies have shown changes in thiol status and thiol/disulphide homeostasis in various diseases such as digestive system, respiratory system, reproductive system, urinary system, metabolic diseases and cancer. This also shows that the thiol state is very important in the pathogenesis of oxidative stress-mediated diseases. Therefore, it is thought that interventions that can improve thiol status may contribute to the prevention or treatment of oxidative stress-related diseases.","PeriodicalId":426818,"journal":{"name":"Lipid Peroxidation [Working Title]","volume":"32 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124798907","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lipid Peroxidation: Aging Kidney","authors":"Harnavi Harun","doi":"10.5772/INTECHOPEN.95801","DOIUrl":"https://doi.org/10.5772/INTECHOPEN.95801","url":null,"abstract":"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 immunolo","PeriodicalId":426818,"journal":{"name":"Lipid Peroxidation [Working Title]","volume":"6 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2021-02-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"124026857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Lipid Peroxidation","authors":"Suzan Onur Yaman, Adnan Ayhancı","doi":"10.32388/1110ak","DOIUrl":"https://doi.org/10.32388/1110ak","url":null,"abstract":"Lipid peroxidation (LPO) is initiated by the attack of free radicals (eg OH ·, O2- and H2O2) on cellular or organelle membranes phospholipids or polyunsaturated fatty acids (PUFA), and with the formation of various types of aldehydes, ketones, alkanes, carboxylic acids and polymerization products. It is an autoxidation process that results. These products are highly reactive with other cellular components and serve as biological markers of LPO. Malondialdehyde (MDA), a toxic aldehyde end product of LPO, causes structural changes that mediate its oxidation, such as fragmentation, modification, and aggregation, especially in DNA and protein. The excessive binding of these reactive aldehydes to cellular proteins alters membrane permeability and electrolyte balance. Degradation of proteins leads to progressive degradation of the biological system mediated by oxidative stress. The chain reaction (CR) of LPO is initiated by the attack of free radicals on the PUFA of the cell membrane to form a carbon centered radical (R*). The O2 · - radical attacks the other lipid molecule to form lipid hydroperoxide (ROOH), thereby spreading the CR and forming the lipid peroxyl radical (ROO). These lipid hydroperoxides severely inhibit membrane functionality by allowing ions such as increased hardness and calcium to leak through the membrane. Damage to the lipid membrane and macromolecule oxidation can result in activation of necrotic or apoptotic tissue death pathways if severe enough.","PeriodicalId":426818,"journal":{"name":"Lipid Peroxidation [Working Title]","volume":"1 1","pages":"0"},"PeriodicalIF":0.0,"publicationDate":"2020-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"128790651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}