Inflammation, Lipid (Per)oxidation, and Redox Regulation

Dias, Irundika H.K.; Milic, Ivana; Heiß, Christian; Ademowo, Opeyemi S; Polidori, Maria Cristina; Devitt, Andrew; Griffiths, Helen R.

doi:10.1089/ars.2020.8022

Cited by 37 publications

(34 citation statements)

References 230 publications

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“…During lipid peroxidation, oxygen molecules are added to the unsaturated fatty acyl chain of non-polar lipids, increasing their water solubility and diffusion towards the membrane surface. Cyclooxygenases or lipoxygenases accessibility for their substrates is boosted, the generation of lipid metabolites linked to inflammation is prompted, and the interaction of specific proteins and receptors recognizing lipid oxidation products is promoted [11][12][13][14][15]. All of these actions are part of the lipid-dependent inflammatory cascade.…”

Section: Introductionmentioning

confidence: 99%

Targeting Lipid Peroxidation for Cancer Treatment

et al. 2020

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Cancer is one of the highest prevalent diseases in humans. The chances of surviving cancer and its prognosis are very dependent on the affected tissue, body location, and stage at which the disease is diagnosed. Researchers and pharmaceutical companies worldwide are pursuing many attempts to look for compounds to treat this malignancy. Most of the current strategies to fight cancer implicate the use of compounds acting on DNA damage checkpoints, non-receptor tyrosine kinases activities, regulators of the hedgehog signaling pathways, and metabolic adaptations placed in cancer. In the last decade, the finding of a lipid peroxidation increase linked to 15-lipoxygenases isoform 1 (15-LOX-1) activity stimulation has been found in specific successful treatments against cancer. This discovery contrasts with the production of other lipid oxidation signatures generated by stimulation of other lipoxygenases such as 5-LOX and 12-LOX, and cyclooxygenase (COX-2) activities, which have been suggested as cancer biomarkers and which inhibitors present anti-tumoral and antiproliferative activities. These findings support the previously proposed role of lipid hydroperoxides and their metabolites as cancer cell mediators. Depletion or promotion of lipid peroxidation is generally related to a specific production source associated with a cancer stage or tissue in which cancer originates. This review highlights the potential therapeutical use of chemical derivatives to stimulate or block specific cellular routes to generate lipid hydroperoxides to treat this disease.

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Section: Introductionmentioning

confidence: 99%

Targeting Lipid Peroxidation for Cancer Treatment

et al. 2020

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“…A study performed by our laboratory also revealed that Gln supplementation reduced the muscle M1/M2 ratio and accelerated muscle regeneration in diabetic mice with limb ischemia [ 11 ]. Inflammation is linked to oxidative stress [ 34 ] and tissue hypoxia [ 35 ]. The anti-inflammatory microenvironment in muscles may have been partly responsible for the reductions in lipid peroxidation and HIF-1α expression observed in the Gln-treated group.…”

Section: Discussionmentioning

confidence: 99%

Protective Effects of Glutamine and Leucine Supplementation on Sepsis-Induced Skeletal Muscle Injuries

Hou

Pai

et al. 2021

IJMS

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This study investigated the effects of l-glutamine (Gln) and/or l-leucine (Leu) administration on sepsis-induced skeletal muscle injuries. C57BL/6J mice were subjected to cecal ligation and puncture to induce polymicrobial sepsis and then given an intraperitoneal injection of Gln, Leu, or Gln plus Leu beginning at 1 h after the operation with re-injections every 24 h. All mice were sacrificed on either day 1 or day 4 after the operation. Blood and muscles were collected for analysis of inflammation and oxidative damage-related biomolecules. Results indicated that both Gln and Leu supplementation alleviated sepsis-induced skeletal muscle damage by reducing monocyte infiltration, calpain activity, and mRNA expression levels of inflammatory cytokines and hypoxia-inducible factor-1α. Furthermore, septic mice treated with Gln had higher percentages of blood anti-inflammatory monocytes and muscle M2 macrophages, whereas Leu treatment enhanced the muscle expressions of mitochondrion-related genes. However, there were no synergistic effects when Gln and Leu were simultaneously administered. These findings suggest that both Gln and Leu had prominent abilities to attenuate inflammation and degradation of skeletal muscles in the early and/or late phases of sepsis. Moreover, Gln promoted the switch of leukocytes toward an anti-inflammatory phenotype, while Leu treatment maintained muscle bioenergetic function.

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“…in the oxidative stress control related to AA and its metabolites. Their activity can also support cells to regulate the AA and its derivatives oxidation and when this system fails, markers related to lipid liporoxidation may appear in the circulation [37][38][39][40]. In contrast to catalases and superoxide dismutases, peroxidases use a thiol-based reaction mechanism to detoxify hydroperoxides and their reduced state needs to be restored through the GSH / GR or Trx / TrxR system under NADPH consumption (or in a special case, NADH) [41,22].…”

Section: Discussionmentioning

confidence: 99%

Evaluation of Thiol-dependent Enzymes on the Pharmacological Effects Induced by the Catalytically Active PLA2 from Bothrops jararacussu

Toyama¹,

Crc²,

Mn³

et al. 2021

Preprint

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Background: Clinical cases reports with snake accidents show that venom bite induces increased oxidative stress including several markers of lipid peroxidation and other oxidative stress marker in plasma. Methods: The main findings of this work were performed with BthTx-II on paw edema of animals treated with the toxin and biochemical measurement of COX-2, PGE2, MDA and the effects of peroxiredoxin inhibitors on edema and myotoxicity were also evaluated. Results: The results show that edema and myotoxocity induced by PLA2 (BthTx-II) induces a strong mobilization of arachidonic acid and an increase in cellular oxidative stress as measured by increased malondialdehydo (MDA) concentration and protein carbonylation. Thus, these findings establish the strong link between oxidative stress, arachidonic acid mobilization and that these events may explain the presence of oxidative stress markers in snake-bitten patients. Experiments performed with animals previously treated with commercially purchased inhibitors showed enzymes such as thioredoxin (TXN), thioredoxin reductase (TXNRD) and other glutathione (GSH)-related antioxidant defenses could play an essential role controlling and defining the end of edema on the late phase of PLA2 BthTx-II-induced process. Conclusion. This study showed that thioate-dependent antioxidant enzymes play an important role in resolving the edema induced by BthTx-II.

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Inflammation, Lipid (Per)oxidation, and Redox Regulation

Cited by 37 publications

References 230 publications

Targeting Lipid Peroxidation for Cancer Treatment

Targeting Lipid Peroxidation for Cancer Treatment

Protective Effects of Glutamine and Leucine Supplementation on Sepsis-Induced Skeletal Muscle Injuries

Evaluation of Thiol-dependent Enzymes on the Pharmacological Effects Induced by the Catalytically Active PLA2 from Bothrops jararacussu

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