Antagonistic role of 9-lipoxygenase-derived oxylipins and ethylene in the control of oxidative stress, lipid peroxidation and plant defence

Rheumatoid arthritis (RA) is a highly debilitating chronic inflammatory autoimmune disease most prevalent in women. The true etiology of this disease is complex, multifactorial, and is yet to be completely elucidated. However, oxidative stress and lipid peroxidation are associated with the development and pathogenesis of RA. In this case, oxidative damage biomarkers have been found to be significantly higher in RA patients, associated with the oxidation of biomolecules and the stimulation of inflammatory responses. Lipid peroxidation is one of the major consequences of oxidative stress, with the formation of deleterious lipid hydroperoxides and electrophilic reactive lipid species. Additionally, changes in the lipoprotein profile seem to be common in RA, contributing to cardiovascular diseases and a chronic inflammatory environment. Nevertheless, changes in the lipid profile at a molecular level in RA are still poorly understood. Therefore, the goal of this review was to gather all the information regarding lipid alterations in RA analyzed by mass spectrometry. Studies on the variation of lipid profile in RA using lipidomics showed that fatty acid and phospholipid metabolisms, especially in phosphatidylcholine and phosphatidylethanolamine, are affected in this disease. These promising results could lead to the discovery of new diagnostic lipid biomarkers for early diagnosis of RA and targets for personalized medicine.

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Introduction: Role of lipid peroxidation and oxidative stress in alcohol toxicity

Free Radical Biology and Medicine ◽

10.1016/0891-5849(89)90029-4 ◽

1989 ◽

Vol 7 (5) ◽

pp. 537-539 ◽

Cited By ~ 120

Author(s):

Arthur I. Cederbaum

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

And Oxidative Stress

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Different Role of Lipid Peroxidation in Oxidative Stress-Induced Lethal Injury in Normal and Tumor Thymocytes

Archives of Biochemistry and Biophysics ◽

10.1006/abbi.1994.1284 ◽

1994 ◽

Vol 312 (1) ◽

pp. 88-94 ◽

Cited By ~ 12

Author(s):

P. Palozza ◽

G. Agostara ◽

E. Piccioni ◽

G.M. Bartoli

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation

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Chronic inflammation and oxidative stress in the genesis and perpetuation of cancer: role of lipid peroxidation, DNA damage, and repair

Langenbeck s Archives of Surgery ◽

10.1007/s00423-006-0073-1 ◽

2006 ◽

Vol 391 (5) ◽

pp. 499-510 ◽

Cited By ~ 277

Author(s):

Helmut Bartsch ◽

Jagadeesan Nair

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Dna Damage ◽

Chronic Inflammation ◽

Dna Damage And Repair ◽

And Oxidative Stress

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Role of AT1 receptors and NAD(P)H oxidase in diabetes-aggravated ischemic brain injury

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.01169.2003 ◽

2004 ◽

Vol 286 (6) ◽

pp. H2442-H2451 ◽

Cited By ~ 92

Author(s):

Ikuyo Kusaka ◽

Gen Kusaka ◽

Changman Zhou ◽

Mami Ishikawa ◽

Anil Nanda ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Brain Injury ◽

Cerebral Ischemia ◽

Cerebral Infarction ◽

Focal Cerebral Ischemia ◽

Lipid Hydroperoxide ◽

Neurological Deficits ◽

Sprague Dawley

The objective of the present study was to examine the role of the angiotensin II type 1 receptor (AT1-R) in the diabetes-aggravated oxidative stress and brain injury observed in a rat model of combined diabetes and focal cerebral ischemia. Diabetes was induced by an injection of streptozotoxin (STZ; 55 mg/kg iv) at 8 wk of age. Two weeks after the induction of diabetes, some animals received continuous subcutaneous infusion of the AT1-R antagonist candesartan (0.5 mg·kg−1·day−1) for 14 days. Focal cerebral ischemia, induced by middle cerebral artery occlusion/reperfusion (MCAO), was conducted at 4 wk after STZ injection. Male Sprague-Dawley rats ( n = 189) were divided into five groups: normal control, diabetes, MCAO, diabetes + MCAO, and diabetes + MCAO + candesartan. The major observations were that 1) MCAO produced typical cerebral infarction and neurological deficits at 24 h that were accompanied by elevation of NAD(P)H oxidase gp91phox and p22phox mRNAs, and lipid hydroperoxide production in the ipsilateral hemisphere; 2) diabetes enhanced NAD(P)H oxidase gp91phox and p22phox mRNA expression, potentiated lipid peroxidation, aggravated neurological deficits, and enlarged cerebral infarction; and 3) candesartan reduced the expression of gp91phox and p22phox, decreased lipid peroxidation, lessened cerebral infarction, and improved the neurological outcome. We conclude that diabetes exaggerates the oxidative stress, NAD(P)H oxidase induction, and brain injury induced by focal cerebral ischemia. The diabetes-aggravated brain injury involves AT1-Rs. We have shown for the first time that candesartan reduces brain injury in a combined model of diabetes and cerebral ischemia.

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The role of lipid peroxidation products and oxidative stress in activation of the canonical wingless-type MMTV integration site (WNT) pathway in a rat model of diabetic retinopathy

Diabetologia ◽

10.1007/s00125-010-1943-1 ◽

2010 ◽

Vol 54 (2) ◽

pp. 459-468 ◽

Cited By ~ 39

Author(s):

T. Zhou ◽

K. K. Zhou ◽

K. Lee ◽

G. Gao ◽

T. J. Lyons ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Diabetic Retinopathy ◽

Rat Model ◽

Wnt Pathway ◽

Integration Site ◽

Lipid Peroxidation Products ◽

And Oxidative Stress

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Sympathetic Nervous System Control of Carbon Tetrachloride-Induced Oxidative Stress in Liver throughα-Adrenergic Signaling

Oxidative Medicine and Cellular Longevity ◽

10.1155/2016/3190617 ◽

2016 ◽

Vol 2016 ◽

pp. 1-11 ◽

Cited By ~ 5

Author(s):

Jung-Chun Lin ◽

Yi-Jen Peng ◽

Shih-Yu Wang ◽

Mei-Ju Lai ◽

Ton-Ho Young ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Nervous System ◽

Carbon Tetrachloride ◽

Sympathetic Nervous System ◽

Nerve Fibers ◽

Adrenergic Signaling ◽

Adrenergic Antagonist ◽

Sympathetic Nervous

In addition to being the primary organ involved in redox cycling, the liver is one of the most highly innervated tissues in mammals. The interaction between hepatocytes and sympathetic, parasympathetic, and peptidergic nerve fibers through a variety of neurotransmitters and signaling pathways is recognized as being important in the regulation of hepatocyte function, liver regeneration, and hepatic fibrosis. However, less is known regarding the role of the sympathetic nervous system (SNS) in modulating the hepatic response to oxidative stress. Our aim was to investigate the role of the SNS in healthy and oxidatively stressed liver parenchyma. Mice treated with 6-hydroxydopamine hydrobromide were used to realize chemical sympathectomy. Carbon tetrachloride (CCl4) injection was used to induce oxidative liver injury. Sympathectomized animals were protected from CCl4induced hepatic lipid peroxidation-mediated cytotoxicity and genotoxicity as assessed by 4-hydroxy-2-nonenal levels, morphological features of cell damage, and DNA oxidative damage. Furthermore, sympathectomy modulated hepatic inflammatory response induced by CCl4-mediated lipid peroxidation. CCl4induced lipid peroxidation and hepatotoxicity were suppressed by administration of anα-adrenergic antagonist. We conclude that the SNS provides a permissive microenvironment for hepatic oxidative stress indicating the possibility that targeting the hepaticα-adrenergic signaling could be a viable strategy for improving outcomes in patients with acute hepatic injury.

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Curcumin Reduce Sodium Fluoride-Induced Oxidative Stress in Rat Brain

Biosciences Biotechnology Research Asia ◽

10.13005/bbra/2609 ◽

2018 ◽

Vol 15 (1) ◽

pp. 71-77 ◽

Cited By ~ 1

Author(s):

Nagapuri Kiran Kumar ◽

Mesram Nageshwar ◽

Karnati Pratap Reddy

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Oxidative Damage ◽

Oral Administration ◽

Rat Brain ◽

Sodium Fluoride ◽

Oxidative Stress Markers ◽

Stress Markers ◽

The Brain

This study reports the ameliorative role of curcumin against sodium fluoride (NaF) induced oxidative stress in the brain of rats. The rats were divided into control, NaF (20 mg/kg), NaF+Curcumin (20mg/kg) and Curcumin (20mg/kg) groups respectively and treated at everyday interval for 60 consecutive days. Oxidative stress markers in the brain were measured at 60th day. NaF treatment significantly increased LPO content, but decreased the level of GSH and activities of SOD, GPx, and CAT the brain of rats in comparison to the control rats. Oral administration of curcumin to fluoride exposed rats significantly reversed the content of lipid peroxidation, as well as enhanced the level of GSH and SOD, GPx and CAT activities to normal compared to NaF exposed rats. Thus, curcumin showed the potential to prevent sodium fluoride induced oxidative damage in the brain of rats and curcumin may be useful agents against neurodegeneration in the brain.

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Mitochondrial, lysosomal and DNA damages induced by acrylamide attenuate by ellagic acid in human lymphocyte

PLoS ONE ◽

10.1371/journal.pone.0247776 ◽

2021 ◽

Vol 16 (2) ◽

pp. e0247776

Author(s):

Ahmad Salimi ◽

Elahe Baghal ◽

Hassan Ghobadi ◽

Niloufar Hashemidanesh ◽

Farzad Khodaparast ◽

...

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Dna Damage ◽

Ellagic Acid ◽

Human Lymphocytes ◽

Health Concern ◽

Cytochrome P450 Enzyme ◽

Dna Damages ◽

Ros Formation

Acrylamide (AA), is an important contaminant formed during food processing under high temperature. Due to its potential neurotoxicity, reproductive toxicity, hepatotoxicity, immunotoxicity, genotoxicity and carcinogenicity effects, this food contaminant has been recognized as a human health concern. Previous studies showed that acrylamide-induced toxicity is associated with active metabolite of acrylamide by cytochrome P450 enzyme, oxidative stress, mitochondrial dysfunction and DNA damage. In the current study, we investigated the role of oxidative stress in acrylamide’s genotoxicity and therapeutic potential role of ellagic acid (EA) in human lymphocytes. Human lymphocytes were simultaneously treated with different concentrations of EA (10, 25 and 50 μM) and acrylamide (50 μM) for 4 h at 37°C. After 4 hours of incubation, the toxicity parameters such cytotoxicity, ROS formation, oxidized/reduced glutathione (GSH/GSSG) content, malondialdehyde (MDA) level, lysosomal membrane integrity, mitochondria membrane potential (ΔΨm) collapse and 8-hydroxy-2’-deoxyguanosine (8-OHdG) were analyzed using biochemical and flow cytometry evaluations. It has been found that acrylamide (50 μM) significantly increased cytotoxicity, ROS formation, GSH oxidation, lipid peroxidation, MMP collapse, lysosomal and DNA damage in human lymphocytes. On the other hand, cotreatment with EA (25 and 50 μM) inhibited AA-induced oxidative stress which subsequently led to decreasing of the cytotoxicity, GSH oxidation, lipid peroxidation, MMP collapse, lysosomal and DNA damage. Together, these results suggest that probably the co-exposure of EA with foods containing acrylamide could decrease mitochondrial, lysosomal and DNA damages, and oxidative stress induced by acrylamide in human body.

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