Lipid peroxidation and its measurement
Roger L. McMullen in Antioxidants and the Skin, 2018
Arachidonic acid is an omega-6 fatty acid that is incorporated into the structure of many phospholipids in eukaryotic cells. In normal metabolic circumstances it is converted to prostaglandins by the enzyme cyclooxygenase (COX). However, during lipid peroxidation arachidonic acid may be converted by a free radical mechanism (COX is not involved) to prostaglandin-like compounds, which belong to the family of isoprostanes and are toxic. Figure 5.11 shows a common F2-isoprostane that is often used as a probe of isoprostane formation. The F2-isoprostanes have become accepted as key biomarkers of oxidative stress in vivo and are usually present in tissues or fluids suffering from oxidative damage at elevated concentrations.103–108
Complementary and integrative treatments I
Kathleen A. Kendall-Tackett in Depression in New Mothers, 2016
EPA and DHA were also used to treat major depression during pregnancy (Su et al., 2008). In this study, 36 pregnant women with major depression participated in a randomized clinical trial comparing a placebo to 3.4 g EPA/DHA (2.2 g DHA, 1.2 g EPA). Compared to the placebo group, subjects in the EPA/DHA group had significantly lower depression scores on the Hamilton Rating Scale for Depression at 6 and 8 weeks than the placebo group, and had a higher (although non-significant) remission rate. EPA and DHA were well tolerated and there were no adverse effects for either mother or baby. The authors noted that this treatment was likely effective because it halted the arachidonic acid cascade. Arachidonic acid is a long-chain, omega-6 fatty acid and is proinflammatory (see Figure 14.1). People with mood disorders often have higher levels of arachidonic acid in their plasma than do those without mood disorders.
Traditional Chinese Medicine Rehabilitation Treatment Techniques for COVID-19
Wenguang Xia, Xiaolin Huang in Rehabilitation from COVID-19, 2021
The occurrence of COVID-19 may be related to elevated inflammatory factor levels or “cytokine storm”; therefore, inhibiting the production of these inflammatory factors is essential for the treatment of COVID-19. Arachidonic acid (AA) mediates the production of various inflammatory factors and is closely related to the occurrence, development, and regression of inflammation. Inhibition of the AA metabolism pathway helps to inhibit the release of inflammatory factors in the body and alleviates cytokine storm. Through screening, Ren Yue et al. found that prescribing huoxiangzhengqi capsule, jinhuqinggan granule, lianhuqingwen capsule, qingfei detoxification decoction, xuebijing injection, retoxing injection, and tanreqing injection have potential inhibitory effects on the AA metabolism pathway and may inhibit the pneumonia caused by COVID-19 by relieving the cytokine storm.
Designing of enzyme inhibitors based on active site specificity: lessons from methyl gallate and its lipoxygenase inhibitory profile
Published in Journal of Receptors and Signal Transduction, 2018
Sharanya C. S., Arun K. G., Vijaytha V., Sabu A., Haridas M.
Inflammation is body’s response to internal and external stimuli to eliminate the aggressor agent and restore normalcy. Mechanism of inflammation involves a sequence of events in which metabolism of arachidonic acid plays a significant role. Prostaglandins are one of the mediators which involved in the complex process of inflammation and are responsible for the cause of pain [1,2]. Arachidonic acid can be metabolized by the cyclooxygenase (COX) pathway to prostaglandins and thromboxane A2 and it can also be metabolized by the lipoxygenase (LOX) pathway to hydroperoxyeicosatetraenoic acids (HPETE’s) and leukotrienes (LT’s). These are important biologically active mediators in variety of inflammatory diseases [3,4]. LOXs are nonheme-iron-containing enzymes. The iron ligand sphere has well been characterized from crystallographic data [5,6] and also by X-ray absorption studies [7,8]. It constitutes a slightly distorted regular octahedron. Its four histidine residues (His361, His366, His541, and His545) and the C-terminal isoleucine residue (Ile663) have been identified as protein–iron ligands. The sixth ligand position appears to be engaged by a water molecule or a hydroxy ion [5]. Lipoxygenases (LOXs) comprise a heterogeneous family of lipid-peroxidizing enzymes, which catalyze the dioxygenation of polyenoic fatty acids to form the equivalent hydroperoxides [9,10]. Mammalian LOXs are concerned in the biosynthesis of mediators of anaphylactic reactions and have also been implicated in cell maturation in the pathogenesis of bronchial asthma, atherosclerosis and osteoporosis [11–16].
The potential for metabolomics in the study and treatment of major depressive disorder and related conditions
Published in Expert Review of Proteomics, 2020
A study of metabolomics, based on GC-MS in the PFC of an LPS-induced mouse model of depression, identified 20 differential metabolites associated with lipid metabolism, such as arachidonic acid and ethanolamine, which were increased, and cholesterol, which was decreased [61]. Another metabolomics study, using GC-MS in the hippocampus of a CUMS-induced rat model of depression, showed the dysregulated metabolism of fatty acids, including hexadecane, arachidonic acid, methyl palmitoleate, and 2-monopalmitin, and glycerophospholipids, including phosphorylethanolamine and ethanolamine [46]. Arachidonic acid is a polyunsaturated fatty acid found among the phospholipids of the cell membranes, which can mediate an inflammatory response. Decreased cholesterol levels can influence the development of cholinergic-rich brain areas and cholinergic transmission [63]. These results indicated that lipid metabolism disturbances are associated with the etiology of depression.
Systemic loxoscelism induced warm autoimmune hemolytic anemia: clinical series and review
Published in Hematology, 2022
Brandon Calhoun, Andrew Moore, Andrew Dickey, D. Matthew Shoemaker
Initially, the bite is painless, and most victims are unaware of having been bitten. Within the first 10 min of envenomation local toxicity and subsequent inflammation occurs. Hyalurondiase and collagenase begin breaking down the extracellular matrix of the surrounding tissue. Additionally, sphingomyelinase and phospholipase begin cleaving cellular membrane phospholipids, thereby yielding sphingomyelin and arachidonic acid, respectfully [6]. Arachidonic acid is then metabolized yielding prostaglandins (PG), thromboxane (TX), and leukotrienes (LT). These compounds, along with proinflammatory cytokines, begin to recruit granulocytes to the area of envenomation. Eventually, the combination of venom components, cellular death, and aggressive inflammatory responses lead to hemorrhagic necrosis and ultimately the formation of dermonecrosis (also known as necrotic arachnidism) (Figure 4(B)). Necrotic arachnidism typically presents as a painful erythematous area that ulcerates and develops a central black eschar (Figure 4(A,B) [8].
Related Knowledge Centers
- Arachidic Acid
- Carboxylic Acid
- Chemical Structure
- Eicosatetraenoic Acid
- Peanut Oil
- Phosphatidylethanolamine
- Phospholipid
- Polyunsaturated Fat
- Omega-6 Fatty Acid
- Cis–Trans Isomerism