Effects of long‐chain <i>N</i>‐acylethanolamines on lipid peroxidation in cardiac mitochondria

Parinandi, Narasimham L.; Schmid, Harald H.O.

doi:10.1016/0014-5793(88)80169-8

Cited by 27 publications

(7 citation statements)

References 15 publications

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“…Since PEA is produced by the brain following ischaemic insult [22], the authors suggested that this compound may act as an endogenous neuroprotective agent. The authors further reported that anandamide not only afforded no isolated rat heart mitochondria with FeSO 4 or FeCl 3 / ADP [86]. Another possibility is that protective effects of AEA and possibly PEA that are more relevant to the situation in vivo may be seen if cAMP levels are raised during the exposure periods [87].…”

Section: Ischaemiamentioning

confidence: 91%

The Palmitoylethanolamide Family: A New Class of Anti-Inflammatory Agents ?

Lambert¹,

Vandevoorde²,

Jonsson³

et al. 2002

CMC

274

202

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The discovery of anandamide as an endogenous ligand for the cannabinoid receptors has led to a resurgence of interest in the fatty acid amides. However, N-palmitoylethanolamine (PEA), a shorter and fully saturated analogue of anandamide, has been known since the fifties. This endogenous compound is a member of the N-acylethanolamines, found in most mammalian tissues. PEA is accumulated during inflammation and has been demonstrated to have a number of anti-inflammatory effects, including beneficial effects in clinically relevant animal models of inflammatory pain. It is now engaged in phase II clinical development, and two studies regarding the treatment of chronic lumbosciatalgia and multiple sclerosis are in progress. However, its precise mechanism of action remains debated. In the present review, the biochemical and pharmacological properties of PEA are discussed, in particular with respect to its analgesic and anti-inflammatory properties.

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Section: Ischaemiamentioning

confidence: 91%

The Palmitoylethanolamide Family: A New Class of Anti-Inflammatory Agents ?

Lambert¹,

Vandevoorde²,

Jonsson³

et al. 2002

CMC

274

202

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“…Among NAEs, OEA, PEA, and AEA appeared to inhibit Cu 2+ -induced in vitro lipid peroxidation in plasma lipoproteins [ 202 ] and cardiac mitochondria [ 207 ], consequently showing antioxidant properties in the pathogenesis of atherosclerosis. Moreover, Zolese and collaborators demonstrated that, depending on its concentration of incubation, PEA exerts both anti-oxidative and pro-oxidative effects on radical-induced oxidation of plasma LDL [ 208 ].…”

Section: Modulation Of Oxidative Stress and Lipid Peroxidation Thrmentioning

confidence: 99%

Modulation of the Oxidative Stress and Lipid Peroxidation by Endocannabinoids and Their Lipid Analogues

et al. 2018

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Growing evidence supports the pivotal role played by oxidative stress in tissue injury development, thus resulting in several pathologies including cardiovascular, renal, neuropsychiatric, and neurodegenerative disorders, all characterized by an altered oxidative status. Reactive oxygen and nitrogen species and lipid peroxidation-derived reactive aldehydes including acrolein, malondialdehyde, and 4-hydroxy-2-nonenal, among others, are the main responsible for cellular and tissue damages occurring in redox-dependent processes. In this scenario, a link between the endocannabinoid system (ECS) and redox homeostasis impairment appears to be crucial. Anandamide and 2-arachidonoylglycerol, the best characterized endocannabinoids, are able to modulate the activity of several antioxidant enzymes through targeting the cannabinoid receptors type 1 and 2 as well as additional receptors such as the transient receptor potential vanilloid 1, the peroxisome proliferator-activated receptor alpha, and the orphan G protein-coupled receptors 18 and 55. Moreover, the endocannabinoids lipid analogues N-acylethanolamines showed to protect cell damage and death from reactive aldehydes-induced oxidative stress by restoring the intracellular oxidants-antioxidants balance. In this review, we will provide a better understanding of the main mechanisms triggered by the cross-talk between the oxidative stress and the ECS, focusing also on the enzymatic and non-enzymatic antioxidants as scavengers of reactive aldehydes and their toxic bioactive adducts.

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“…Moreover, OEA and PEA appeared to inhibit Cu 2+ -induced in vitro lipid peroxidation of plasma lipoproteins 12 and cardiac mitochondria. 61 All these evidences could contribute to explain the increase of lag time and the decrease of Ox-LDL found in this clinical trial.…”

Section: Discussionmentioning

confidence: 59%

N-Oleoyl-Phosphatidyl-Ethanolamine and Epigallo Catechin-3-Gallate Mitigate Oxidative Stress in Overweight and Class I Obese People on a Low-Calorie Diet

Cazzola

Rondanelli

2020

Journal of Medicinal Food

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Oxidative stress and lipid peroxidation are considered key factors linking obesity with its associated complications. Epigallo catechin-3-gallate (EGCG) and oleoylethanolamide, together with its phospholipid precursor N-oleoylphosphatidylethanolamine (NOPE), are nutritional compounds that might improve the oxidative stress status of obese people. Unfortunately, the bioavailability of these compounds is low; however, the coadministration of NOPE with EGCG has been shown to ameliorate both the plasma availability of EGCG and the intestinal levels of NOPE in rats. This double-blind placebo-controlled study investigated the effects of 2 months' supplementation with EGCG complexed with NOPE, combined with moderate energy restriction, on plasma oxidative status of overweight and class I obese subjects. A total of 138 subjects (body mass index: 25-35 kg/m 2 ) were recruited and randomized into two groups: the first (n = 67) received caps of placebo and the second (n = 71) caps of an oily dispersion of EGCG complexed with NOPE for 2 months. Subjects' supplementation was combined with moderate energy restriction (-800 kcal/day). Plasma oxidative status was determined by measuring the levels of oxidized low-density lipoprotein (Ox-LDL), malondialdehyde and reactive oxygen metabolites, and by calculating the lag time and the slope of Cu-induced lipid peroxidation kinetics. In total 116 subjects (27 M/89 F) completed the supplementation period, 49 in the placebo group and 67 in the treated group. Treatment induced a similar significant weight reduction in the two groups. Moreover, we found the mean changes of Ox-LDL significantly lower and the mean changes of antioxidant capacity (lag time) significantly higher in NOPE-EGCG group than in placebo group (treatment effect mean difference: -3.15 UL, P < .044 and +5.37 min, P < .0347, respectively). EGCG plasma levels were detectable only after 2 months of NOPE-EGCG diet. The NOPE-EGCG integration to a low-energy diet seems, therefore, useful for ameliorating oxidative stressrelated markers, which are concomitant causes of obesity-induced disorders.

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Effects of long‐chain N‐acylethanolamines on lipid peroxidation in cardiac mitochondria

Cited by 27 publications

References 15 publications

The Palmitoylethanolamide Family: A New Class of Anti-Inflammatory Agents ?

The Palmitoylethanolamide Family: A New Class of Anti-Inflammatory Agents ?

Modulation of the Oxidative Stress and Lipid Peroxidation by Endocannabinoids and Their Lipid Analogues

N-Oleoyl-Phosphatidyl-Ethanolamine and Epigallo Catechin-3-Gallate Mitigate Oxidative Stress in Overweight and Class I Obese People on a Low-Calorie Diet

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