Polyunsaturated Fatty Acids Induce ROS Synthesis in Microvascular Endothelial Cells

Trommer, Simon; Leimert, Anja; Bucher, Michael; Schümann, Julia

doi:10.1007/978-3-319-91287-5_63

Cited by 7 publications

(4 citation statements)

References 7 publications

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“…11d-h). These observations are consistent with recent reports that abundant PUFAs induce cell death by serving as substrates for lipid peroxidation 26,27 , whereas MUFAs decrease lipid peroxidation 28,29 .…”

Section: Complex I Inhibition Identifies a Latent Vulnerability In A ...supporting

confidence: 93%

Ether phospholipids are required for mitochondrial reactive oxygen species homeostasis

Chen

Soeung

et al. 2023

Nat Commun

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Mitochondria are hubs where bioenergetics, redox homeostasis, and anabolic metabolism pathways integrate through a tightly coordinated flux of metabolites. The contributions of mitochondrial metabolism to tumor growth and therapy resistance are evident, but drugs targeting mitochondrial metabolism have repeatedly failed in the clinic. Our study in pancreatic ductal adenocarcinoma (PDAC) finds that cellular and mitochondrial lipid composition influence cancer cell sensitivity to pharmacological inhibition of electron transport chain complex I. Profiling of patient-derived PDAC models revealed that monounsaturated fatty acids (MUFAs) and MUFA-linked ether phospholipids play a critical role in maintaining ROS homeostasis. We show that ether phospholipids support mitochondrial supercomplex assembly and ROS production; accordingly, blocking de novo ether phospholipid biosynthesis sensitized PDAC cells to complex I inhibition by inducing mitochondrial ROS and lipid peroxidation. These data identify ether phospholipids as a regulator of mitochondrial redox control that contributes to the sensitivity of PDAC cells to complex I inhibition.

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Section: Complex I Inhibition Identifies a Latent Vulnerability In A ...supporting

confidence: 93%

Ether phospholipids are required for mitochondrial reactive oxygen species homeostasis

Chen

Soeung

et al. 2023

Nat Commun

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“…This phenomenon may be attributed to the different proportions of fatty acids on the cell membrane. Increasing evidence suggests that increased double bonds in PUFAs in cellular lipids mediate oxidative stress induced by free radicals [42,43]. Lymphocytes have a relatively high content of free fatty acids in their cell membranes, making them more susceptible to peroxidative damage [44].…”

Section: Discussionmentioning

confidence: 99%

The Protective Role of Vitamin E against Oxidative Stress and Immunosuppression Induced by Non-Esterified Fatty Acids in Bovine Peripheral Blood Leukocytes

Li,

Lin,

Moonmanee

et al. 2024

Animals

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High levels of non-esterified fatty acids (NEFAs) during the transition period lead to increased oxidative stress and immunosuppression in cows. Feeding them a vitamin-E-supplemented diet reduces reactive oxygen species (ROS) levels in the blood and diminishes immunosuppression in the transition period. However, whether the restoration of immune cell function occurs through the direct action of vitamin E in cells is still a topic that requires further discussion. Therefore, in this experiment, we aimed to investigate the effect of NEFAs on peripheral blood leukocytes (PBLs) and whether vitamin E mitigates the impact of NEFAs. We employed three groups: (1) blank, (2) NEFA only, and (3) pre-culturing with vitamin E before NEFA treatment (VENEFA). In peripheral blood mononuclear cells (PBMCs), there were no differences in vitamin E content among the three groups. However, in the vitamin E pre-treatment group, the vitamin E levels of polymorphonuclear neutrophils (PMNs) were significantly higher than those in the other two groups. NEFA levels increased malondialdehyde (MDA) levels in PBMCs, but pre-treatment with vitamin E reduced accumulation of MDA levels. Regarding the expression of proinflammatory genes, NEFAs increased the expression of interleukin-1β in PBMCs and colony-stimulating factor 2 in PMNs. Vitamin E pre-treatment restored the increase in interleukin-1β levels caused by NEFAs in PBMCs. None of the groups affected the phagocytosis of PMNs. Few studies have confirmed that NEFAs cause oxidative stress in bovine PBLs. In summary, this study found that NEFAs induce oxidative stress in PBLs and alter the expression of inflammation-related genes; meanwhile, vitamin E can reduce some of the effects caused by NEFAs. This result may suggest that vitamin E can assist bovine PBLs in resisting the immune suppression caused by an NEB during the transition period.

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“…According to the results of RNA sequencing, ZZDX could affect the pathways of unsaturated fatty acids biosynthesis, fatty acid elongation, and fatty acid metabolism. These pathways have been reported to be associated with ROS formation and can induce inflammation [ 32 , 33 ]. The levels of ELOVL4, ACOT1 and SCD1 were significantly decreased after ZZDX treatment.…”

Section: Discussionmentioning

confidence: 99%

The tibetan medicine Zuozhu-Daxi can prevent Helicobacter pylori induced-gastric mucosa inflammation by inhibiting lipid metabolism

et al. 2022

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Background Tibetan medicine has been used in clinical practice for more than 3800 years. Zuozhu-Daxi (ZZDX), a classic traditional Tibetan medicine, has been proved to be effective in the treatment of digestive diseases, such as chronic gastritis, gastric ulcer, etc. Helicobacter pylori (H. pylori), one of the most common pathogenic microbes, is regarded as the most common cause of gastritis. Researching on the effects of ZZDX on H. pylori-induced gastric mucosa inflammation could provide more evidences on H. pylori treatment and promote the development of Tibetan medicine. This study aimed to explore whether ZZDX could rescue H. pylori-induced gastric mucosa inflammation and its mechanism. Methods Male C57BL/6 mice were infected with H. pylori, and orally treated with ZZDX to rescue gastric mucosa inflammation induced by H. pylori infection. Pathology of gastric mucosa inflammation was evaluated under microscopy by hematoxylin–eosin (HE) staining. The infection status of H. pylori was evaluated by immunohistochemical (IHC) staining. The reactive oxygen species (ROS) level in serum was evaluated using a detection kit. IL-1α, IL-6, and PGE2 expression levels in serum were measured using ELISA. IL-1α, IL-8, TNF-α, and NOD1 expression levels in gastric tissues were measured using real-time PCR. RNA sequencing and gene certification of interest were performed to explore the mechanisms in vivo and in vitro. Results The results showed that ZZDX could significantly inhibit H. pylori-induced gastric mucosa inflammation using HE staining. IL-1α, IL-6, and PGE2 expression levels in serum were significantly decreased after treatment with ZZDX. ZZDX treatment significantly decreased the mRNA expression of IL-8 induced by H. pylori infection in gastric tissues. Elovl4, Acot1 and Scd1 might be involved in the mechanisms of ZZDX treatment. However, the H. pylori infection status in the gastric mucosa was not reduced after ZZDX treatment. Conclusions ZZDX reversed gastric mucosal injury and alleviated gastric mucosa inflammation induced by H. pylori infection.

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Polyunsaturated Fatty Acids Induce ROS Synthesis in Microvascular Endothelial Cells

Cited by 7 publications

References 7 publications

Ether phospholipids are required for mitochondrial reactive oxygen species homeostasis

Ether phospholipids are required for mitochondrial reactive oxygen species homeostasis

The Protective Role of Vitamin E against Oxidative Stress and Immunosuppression Induced by Non-Esterified Fatty Acids in Bovine Peripheral Blood Leukocytes

The tibetan medicine Zuozhu-Daxi can prevent Helicobacter pylori induced-gastric mucosa inflammation by inhibiting lipid metabolism

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