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Omega-3 and Omega-6 Fatty Acids*
Published in Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss, Nutrition and Cardiometabolic Health, 2017
William S. Harris, Nathalie Bergeron, Patty W. Siri-Tarino, George A. Bray, Ronald M. Krauss
As noted, the “LA is harmful” hypothesis depends heavily on the view that an LA metabolite, AA, is converted to potent pro-inflammatory signaling molecules. While this is partly true, what is often overlooked is that AA also gives rise to anti-inflammatory metabolites (e.g., lipoxin A4), as well as anti-aggregatory, vasodilative molecules like prostacyclin. Indeed, the epoxyeicosatrienoic acids synthesized from AA produce vasodilation, stimulate angiogenesis, have anti-inflammatory actions, and protect the heart against ischemia–reperfusion injury (Spector, 2009). AA can be converted into an ever-expanding list of bioactive compounds via cyclooxygenase, lipoxygenases, and cytochrome P450 monooxygenases (Figure 10.2a). But AA is not the only omega-6 FA with potential effects on CHD—LA itself can be converted to a wide variety of bioactive molecules by these enzymes (Figure 10.2a). Not shown in this figure is nitrated LA (LNO2), an LA metabolite that has been shown to have cardioprotective effects (Baker et al., 2009). In addition, LNO2 is a powerful ligand for peroxisome proliferator activator receptor-gamma (PPAR-γ) (Schopfer et al., 2005), a nuclear transcription factor that controls cell differentiation as well as production of metabolic and anti-inflammatory signaling molecules. At physiologically relevant levels, LNO2 rivals the effects of the thiazolidinediones on PPAR-γ (Schopfer et al., 2005). LA can also be converted to a growing number of oxygenated metabolites (i.e., oxylipins) by cyclooxygenase, lipoxygenases, and/or cytochrome P-450 epoxygenases (Figure 10.2a), the individual and aggregate effects of which have not been systematically examined.
Predictive serum biomarkers of patients with cerebral infarction
Published in Neurological Research, 2022
Yan Kong, Yu-qing Feng, Ya-ting Lu, Shi-sui Feng, Zheng Huang, Qian-yi Wang, Hui-min Huang, Xue Ling, Zhi-heng Su, Yue Guo
Arachidonic acid (AA) is a type of unsaturated fatty acid that has the widest distribution and highest content in the human body. It is the precursor of many important active cardiovascular and cerebrovascular substances in the human body. A variety of AA metabolites that are regulated by AA metabolism genes are related to the formation of atherosclerotic plaques and the pathogenesis of cerebral infarction. The metabolism of AA is always dynamic, and once its balance is destroyed, atherosclerosis and cerebral infarction occur. AA is involved in three metabolic pathways: cyclooxygenase, lipoxygenase, and cytochrome P450 (CYP) [24,25]. Among these, the third metabolic pathway, CYP cyclooxygenase, catalyzes AA into epoxyeicosatrienoic acids (EETs), which has functions of anti-inflammation, lowering of blood pressure, attenuation of ischemia-reperfusion injury of the myocardium, and reduction of the infarct area of the myocardium and brain tissue [26]. Cerebral inflammation plays a crucial role in the pathophysiology of ischemic stroke and involves all stages of the ischemic cascade [27]. We showed that the level of 5,6-epoxy-8,11,14-eicosatrienoic acid in the serum of patients with cerebral infarction was significantly higher than that of the control group. We hypothesized that AA is converted into EET under the catalysis of the CYP2 enzyme to a greater degree with the occurrence of cerebral inflammation during cerebral infarction. Therefore, AA metabolism dysfunction may be another pathogenesis of cerebral infarction. Patients with cerebral infarction may be treated by stabilizing AA metabolism.
Vascular endothelial damage in COPD: current functional assessment methods and future perspectives
Published in Expert Review of Respiratory Medicine, 2021
Marieta P. Theodorakopoulou, Dimitra Rafailia Bakaloudi, Konstantina Dipla, Andreas Zafeiridis, Afroditi K. Boutou
In a previous study in patients with COPD, Maclay et al. showed that endothelium-dependent and endothelium-independent vasodilation assessed with VOP did not significantly differentiate between 18 COPD patients and 17 healthy controls, despite that COPD was independently associated with increased arterial stiffness [17]. In another study, FBF was not different between normocythemic and polycythemic COPD patients at rest and after bradykinin (endothelium-dependent vasodilation) or nitroprusside (endothelium-independent vasodilation) infusion [18]. However, in the same study, acetylcholine-induced vasodilation was markedly declined in polycythemic patients and it was inversely correlated with the hemoglobin levels, suggesting that polycythemia is predominantly associated with microvascular endothelial dysfunction [18]. In contrast to the above, Yang et al. demonstrated that patients with COPD and overweight smokers have impaired endothelial function, as assessed by VOP, and dysregulated epoxyeicosatrienoic acid production (an endothelium-derived hyperpolarizing factor, acting as vasodilator [19]); inhibition of soluble epoxide hydrolase alters epoxyeicosatrienoic acid metabolism and augments bradykinin-induced vasodilation in forearm resistance vessels, both in vitro and in vivo in these subjects [20].
Omega‐3 Polyunsaturated Fatty Acids and Lung Cancer: nutrition or Pharmacology?
Published in Nutrition and Cancer, 2021
Owen M. Vega, Shaheen Abkenari, Zhen Tong, Austin Tedman, Sara Huerta-Yepez
In addition, to the COX pathway, ω-3 and ω-6 PUFAs are substrates of multiple pathways including the LOX and cytochrome P450 epoxygenases (96, 97). CYP epoxygenase produce epoxyeicosatrienoic acids (EETs) through the ω-6 PUFA, AA. These enzymes also produce epoxy docosapentaenoic acids (EDPs) through the ω-3 PUFA, DHA. AA and DHA therefore compete for CYP epoxygenase activity (98). Zhang, G et al. looked at the effects of EDPs produced from DHA, on tumor growth. They performed an experiment on C57BL/6 mice to investigate the effects of EDPs and EETs on metastasis using the LLC cell line. When EDPs and EETs were co-administered with an epoxide hydrolase inhibitor, trans-4-[4-(3-adamantan-1-yl-ureido)-cyclohexyloxy]-benzoic acid (t-AUCB), EDP inhibited tumor metastasis whereas EET increased tumor metastasis. The role of the epoxide hydrolase inhibitor elevated levels of ω-3 and ω-6 metabolites exaggerating their effects. The results of this experiment suggest that increased levels of ω-3 PUFA metabolites have a positive effect on mice by decreasing lung cancer metastasis. Conversely, the opposite effect is seen with an ω-6 diet.