scholarly journals The α6β4 integrin promotes resistance to ferroptosis

2017 ◽  
Vol 216 (12) ◽  
pp. 4287-4297 ◽  
Author(s):  
Caitlin W. Brown ◽  
John J. Amante ◽  
Hira Lal Goel ◽  
Arthur M. Mercurio
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Extracellular Matrix ◽  
Cancer Biology ◽  
Membrane Lipids ◽  
Lipid Peroxides ◽  
Causal Link ◽  
Carcinoma Cells ◽  
Adherent Cells ◽  
Α6β4 Integrin

Increases in lipid peroxidation can cause ferroptosis, a form of cell death triggered by inhibition of glutathione peroxidase 4 (GPX4), which catalyzes the reduction of lipid peroxides and is a target of ferroptosis inducers, such as erastin. The α6β4 integrin protects adherent epithelial and carcinoma cells from ferroptosis induced by erastin. In addition, extracellular matrix (ECM) detachment is a physiologic trigger of ferroptosis, which is evaded by α6β4. The mechanism that enables α6β4 to evade ferroptosis involves its ability to protect changes in membrane lipids that are proferroptotic. Specifically, α6β4-mediated activation of Src and STAT3 suppresses expression of ACSL4, an enzyme that enriches membranes with long polyunsaturated fatty acids and is required for ferroptosis. Adherent cells lacking α6β4 require an inducer, such as erastin, to undergo ferroptosis because they sustain GPX4 expression, despite their increase in ACSL4. In contrast, ECM detachment of cells lacking α6β4 is sufficient to trigger ferroptosis because GPX4 is suppressed. This causal link between α6β4 and ferroptosis has implications for cancer biology and therapy.

Superresistance against hypoxia after preliminary adaptation to repeated stress

1994 ◽  
Vol 76 (5) ◽  
pp. 1856-1861 ◽  
Author(s):  
F. Meerson ◽  
V. Pozharov ◽  
T. Minyailenko
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Protective Effect ◽  
Tidal Volume ◽  
Restraint Stress ◽  
Lipid Peroxides ◽  
Alveolar Ventilation ◽  
O2 Consumption ◽  
Adaptation To Stress ◽  
Resistance To Hypoxia

The study investigated the influence of adaptation to stress on resistance to hypoxia. After rats were adaptated to moderate restraint stress, they were anesthetized and exposed to 6% O2. Adaptation increased tidal volume by 2.6-fold, lung and alveolar ventilation by 1.6- and 1.8-fold, respectively, and O2 consumption by 1.6-fold; limited lactate accumulation in the liver by 2-fold, in the heart by 34%, in the lung by 36%, and in the blood by 36%; and elevated pH. At the same time, preliminary adaptation to stress inhibited the hypoxic activation of lipolysis and peroxidation in all tissues. The concentration of lipid peroxides decreased after adaptation by 1.3- to 1.5-fold in different organs, whereas the content of free fatty acids diminished by 1.7- to 2.3-fold. Finally, after adaptation, mortality decreased under severe hypoxia by 6.5-fold. Thus, the data suggest that the cross-protective effect of adaptation was achieved by the economization of respiration and circulation, by marked augmentation in the ability of tissue to utilize blood O2, and by the limitation of processes that are able to damage tissue membranes, namely, acidosis, lipolysis, and lipid peroxidation.

De la peroxydation lipidique radioinduite : les facteurs déterminant l'oxydabilité des lipides

2001 ◽  
Vol 79 (2) ◽  
pp. 144-153 ◽  
Author(s):  
Samy Rémita
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Membrane Lipids ◽  
Membrane Damage ◽  
Chain Reaction ◽  
Amphiphilic Molecules ◽  
Essential Components ◽  
Radiation Induced ◽  
A Chain ◽  
Peroxydation Lipidique

Lipids are the essential components of cell membranes and lipoproteins. Their peroxidation plays an important role in numerous pathologies in which oxidative stress is involved. Lipid peroxidation occurs through a chain reaction that contributes to membrane damage in cells. It results in the conversion of fatty acids to polar hydroperoxides and leads to the breakdown or malfunction of the membrane. Lipids are amphiphilic molecules that aggregate in aqueous solutions into micelles and liposoms. The effect of this structural organization is significant in studies of radiation-induced peroxidation damage in highly ordered biological systems such as biological membranes. In this paper, a synthesis of the data concerning radioinduced lipid peroxidation is completed by an original review of the different parameters that determine lipid oxidizability. In addition, the influence of lipid aggregation and the effect of molecular packing are discussed.Key words: radiolysis, peroxidation, lipids, fatty acids.

Melatonin reduces high levels of lipid peroxidation induced by potassium iodate in porcine thyroid

2019 ◽  
pp. 1-7 ◽  
Author(s):  
Paulina Iwan ◽  
Jan Stepniak ◽  
Malgorzata Karbownik-Lewinska
Keyword(s):  
Lipid Peroxidation ◽  
Oxidative Damage ◽  
Membrane Lipids ◽  
Chemical Properties ◽  
Iodine Concentration ◽  
Free Radical Scavenger ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Potassium Iodate ◽  
Hormone Synthesis

Abstract. Iodine is essential for thyroid hormone synthesis. Under normal iodine supply, calculated physiological iodine concentration in the thyroid is approx. 9 mM. Either potassium iodide (KI) or potassium iodate (KIO3) are used in iodine prophylaxis. KI is confirmed as absolutely safe. KIO3 possesses chemical properties suggesting its potential toxicity. Melatonin (N-acetyl-5-methoxytryptamine) is an effective antioxidant and free radical scavenger. Study aims: to evaluate potential protective effects of melatonin against oxidative damage to membrane lipids (lipid peroxidation, LPO) induced by KI or KIO3 in porcine thyroid. Homogenates of twenty four (24) thyroids were incubated in presence of either KI or KIO3 without/with melatonin (5 mM). As melatonin was not effective against KI-induced LPO, in the next step only KIO3 was used. Homogenates were incubated in presence of KIO3 (200; 100; 50; 25; 20; 15; 10; 7.5; 5.0; 2.5; 1.25 mM) without/with melatonin or 17ß-estradiol. Five experiments were performed with different concentrations of melatonin (5.0; 2.5; 1.25; 1.0; 0.625 mM) and one with 17ß-estradiol (1.0 mM). Malondialdehyde + 4-hydroxyalkenals (MDA + 4-HDA) concentration (LPO index) was measured spectrophotometrically. KIO3 increased LPO with the strongest damaging effect (MDA + 4-HDA level: ≈1.28 nmol/mg protein, p < 0.05) revealed at concentrations of around 15 mM, thus corresponding to physiological iodine concentrations in the thyroid. Melatonin reduced LPO (MDA + 4-HDA levels: from ≈0.97 to ≈0,76 and from ≈0,64 to ≈0,49 nmol/mg protein, p < 0.05) induced by KIO3 at concentrations of 10 mM or 7.5 mM. Conclusion: Melatonin can reduce very strong oxidative damage to membrane lipids caused by KIO3 used in doses resulting in physiological iodine concentrations in the thyroid.

Lipid Profile of Pig Tissues Contrasting in Meat Production

2019 ◽  
Vol 09 ◽  
Author(s):  
Vitaly A. Bekenev ◽  
Anatoly A. Arishin ◽  
Sergei N. Mager ◽  
Izolda V. Bolshakova ◽  
Natalia L. Tretyakova ◽  
...  
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Linoleic Acid ◽  
Live Weight ◽  
Blood Lipid ◽  
Meat Production ◽  
Thoracic Vertebrae ◽  
Organoleptic Properties ◽  
Biochemical Characteristics

Background: Studies were carried out on two breeds of pigs - Pietrain (P), and Kemerovo (K), contrasting in composition of carcasses, and their hybrids. Objective: The purpose of this work was to establish the characteristics of the composition of lipids of intramuscular fat (IMF), back fat and serum, organoleptic qualities in animals of these breeds. Methods: Animals of 10 individuals in each group were fed on a standard feed and slaughtered with a live weight of 95-100 kg. The quality of carcasses, the biochemical characteristics of blood, the composition of fatty acids and cholesterol in meat and fat, and blood lipid peroxidation were determined. Results: Thickness on the back fat (BF) at the level of 6-7 thoracic vertebrae with a live weight of 100 kg was 35.8 ± 1.65 mm in pigs of breed K, in hybrids - 27.6 ± 1.06, and in breed P - 19, 6 ± 1.43 mm. IMF in pigs of breed K was almost 4.5 times greater than that of breed P. IMF K breed contained 2 times less cholesterol than in P (2.34 vs. 4.68%). In the IMF, K was 2 times less polyunsaturated fatty acids (PUFA), than P, 7.82 and 15.22%, linoleic acid, 6.74% and 12.42% respectively (p &lt;0.005).The organoleptic properties of meat and salted back fat were significantly higher in breed K (P = 0.05). Conclusion: The data obtained allow us to establish priorities in the use of products of specific breeds of pigs, depending on medical requirements.

scholarly journals Heat stress elicits remodeling in the anther lipidome of peanut

2020 ◽  
Vol 10 (1) ◽  
Author(s):  
Zolian S. Zoong Lwe ◽  
Ruth Welti ◽  
Daniel Anco ◽  
Salman Naveed ◽  
Sachin Rustgi ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Heat Stress ◽  
Fatty Acid ◽  
Membrane Lipids ◽  
Fatty Acid Desaturase ◽  
Susceptible Genotype ◽  
Unsaturated Lipid ◽  
Lipid Species ◽  
Lipid Unsaturation ◽  
Fatty Acid Amount

AbstractUnderstanding the changes in peanut (Arachis hypogaea L.) anther lipidome under heat stress (HT) will aid in understanding the mechanisms of heat tolerance. We profiled the anther lipidome of seven genotypes exposed to ambient temperature (AT) or HT during flowering. Under AT and HT, the lipidome was dominated by phosphatidylcholine (PC), phosphatidylethanolamine (PE), and triacylglycerol (TAG) species (> 50% of total lipids). Of 89 lipid analytes specified by total acyl carbons:total carbon–carbon double bonds, 36:6, 36:5, and 34:3 PC and 34:3 PE (all contain 18:3 fatty acid and decreased under HT) were the most important lipids that differentiated HT from AT. Heat stress caused decreases in unsaturation indices of membrane lipids, primarily due to decreases in highly-unsaturated lipid species that contained 18:3 fatty acids. In parallel, the expression of Fatty Acid Desaturase 3-2 (FAD3-2; converts 18:2 fatty acids to 18:3) decreased under HT for the heat-tolerant genotype SPT 06-07 but not for the susceptible genotype Bailey. Our results suggested that decreasing lipid unsaturation levels by lowering 18:3 fatty-acid amount through reducing FAD3 expression is likely an acclimation mechanism to heat stress in peanut. Thus, genotypes that are more efficient in doing so will be relatively more tolerant to HT.

scholarly journals Effect of polyunsaturated fatty acids and antioxidants on lipid peroxidation in tissue cultures.

1981 ◽  
Vol 22 (5) ◽  
pp. 763-769
Author(s):  
V C Gavino ◽  
J S Miller ◽  
S O Ikharebha ◽  
G E Milo ◽  
D G Cornwell
Keyword(s):  
Lipid Peroxidation ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Tissue Cultures

scholarly journals Lipidomics Provides New Insight into Pathogenesis and Therapeutic Targets of the Ischemia—Reperfusion Injury

2021 ◽  
Vol 22 (6) ◽  
pp. 2798
Author(s):  
Zoran Todorović ◽  
Siniša Đurašević ◽  
Maja Stojković ◽  
Ilijana Grigorov ◽  
Slađan Pavlović ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Time Course ◽  
Membrane Lipids ◽  
Lipid Analysis ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Enzyme Inactivation ◽  
Critical Event ◽  
Tissue Ischemia ◽  
Insight Into

Lipids play an essential role in both tissue protection and damage. Tissue ischemia creates anaerobic conditions in which enzyme inactivation occurs, and reperfusion can initiate oxidative stress that leads to harmful changes in membrane lipids, the formation of aldehydes, and chain damage until cell death. The critical event in such a series of harmful events in the cell is the unwanted accumulation of fatty acids that leads to lipotoxicity. Lipid analysis provides additional insight into the pathogenesis of ischemia/reperfusion (I/R) disorders and reveals new targets for drug action. The profile of changes in the composition of fatty acids in the cell, as well as the time course of these changes, indicate both the mechanism of damage and new therapeutic possibilities. A therapeutic approach to reperfusion lipotoxicity involves attenuation of fatty acids overload, i.e., their transport to adipose tissue and/or inhibition of the adverse effects of fatty acids on cell damage and death. The latter option involves using PPAR agonists and drugs that modulate the transport of fatty acids via carnitine into the interior of the mitochondria or the redirection of long-chain fatty acids to peroxisomes.

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