Pulmonary lipid peroxides and fatty acids of rats fed different lipids and exposed to oxygen at hyperbaric pressure

Lipids ◽  
1985 ◽  
Vol 20 (4) ◽  
pp. 248-251 ◽  
Author(s):  
Syed Q. Alam ◽  
Bassima S. alam
Keyword(s):  
Fatty Acids ◽  
Lipid Peroxides ◽  
Hyperbaric Pressure

scholarly journals DGAT1 is a lipid metabolism oncoprotein that enables cancer cells to accumulate fatty acid while avoiding lipotoxicity

2020 ◽  
Author(s):  
Daniel J. Wilcock ◽  
Andrew P. Badrock ◽  
Rhys Owen ◽  
Melissa Guerin ◽  
Andrew D. Southam ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Cell Growth ◽  
Cancer Cells ◽  
Melanoma Cell ◽  
Drug Targets ◽  
Lipid Peroxides ◽  
Acid Oxidation ◽  
Growth Factor Signaling ◽  
Bona Fide

ABSTRACTDysregulated cellular metabolism is a hallmark of cancer. As yet, few druggable oncoproteins directly responsible for this hallmark have been identified. Increased fatty acid acquisition allows cancer cells to meet their membrane biogenesis, ATP, and signaling needs. Excess fatty acids suppress growth factor signaling and cause oxidative stress in non-transformed cells, but surprisingly not in cancer cells. Molecules underlying this cancer adaptation may provide new drug targets. Here, we identify Diacylglycerol O-acyltransferase 1 (DGAT1), an enzyme integral to triacylglyceride synthesis and lipid droplet formation, as a frequently up-regulated oncoprotein allowing cancer cells to tolerate excess fatty acids. DGAT1 over-expression alone induced melanoma in zebrafish melanocytes, and co-operated with oncogenic BRAF or NRAS for more rapid melanoma formation. Mechanistically, DGAT1 stimulated melanoma cell growth through sustaining mTOR kinase–S6 kinase signaling and suppressed cell death by tempering fatty acid oxidation, thereby preventing accumulation of reactive oxygen species including lipid peroxides.SIGNIFICANCEWe show that DGAT1 is a bona fide oncoprotein capable of inducing melanoma formation and co-operating with other known drivers of melanoma. DGAT1 facilitates enhanced fatty acid acquisition by melanoma cells through suppressing lipototoxicity. DGAT1 is also critical for maintaining S6K activity required for melanoma cell growth.

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.

scholarly journals Is Ferroptosis a Key Component of the Process Leading to Multiorgan Damage in COVID-19?

Antioxidants ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 1677
Author(s):  
Anna Maria Fratta Pasini ◽  
Chiara Stranieri ◽  
Domenico Girelli ◽  
Fabiana Busti ◽  
Luciano Cominacini
Keyword(s):  
Reactive Oxygen Species ◽  
Fatty Acids ◽  
Cell Death ◽  
Cardiogenic Shock ◽  
Molecular Mechanisms ◽  
Lipid Peroxides ◽  
Oxygen Species ◽  
Intracellular Iron ◽  
Multiple Organs ◽  
Respiratory Pathology

Even though COVID-19 is mostly well-known for affecting respiratory pathology, it can also result in several extrapulmonary manifestations, leading to multiorgan damage. A recent reported case of SARS-CoV-2 myocarditis with cardiogenic shock showed a signature of myocardial and kidney ferroptosis, a novel, iron-dependent programmed cell death. The term ferroptosis was coined in the last decade to describe the form of cell death induced by the small molecule erastin. As a specific inducer of ferroptosis, erastin inhibits cystine-glutamate antiporter system Xc-, blocking transportation into the cytoplasm of cystine, a precursor of glutathione (GSH) in exchange with glutamate and the consequent malfunction of GPX4. Ferroptosis is also promoted by intracellular iron overload and by the iron-dependent accumulation of polyunsaturated fatty acids (PUFA)-derived lipid peroxides. Since depletion of GSH, inactivation of GPX4, altered iron metabolism, and upregulation of PUFA peroxidation by reactive oxygen species are peculiar signs of COVID-19, there is the possibility that SARS-CoV-2 may trigger ferroptosis in the cells of multiple organs, thus contributing to multiorgan damage. Here, we review the molecular mechanisms of ferroptosis and its possible relationship with SARS-CoV-2 infection and multiorgan damage. Finally, we analyze the potential interventions that may combat ferroptosis and, therefore, reduce multiorgan damage.

Effect of transient ischemia on free fatty acids and phospholipids in the gerbil brain

1980 ◽  
Vol 53 (3) ◽  
pp. 323-331 ◽  
Author(s):  
Shinichi Yoshida ◽  
Satoshi Inoh ◽  
Takao Asano ◽  
Keiji Sano ◽  
Masaru Kubota ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Saturated Fatty Acids ◽  
Hydrolytic Enzymes ◽  
Lipid Peroxides ◽  
Thiobarbituric Acid ◽  
Mitochondrial Respiratory Chain ◽  
Membrane Phospholipids ◽  
Content Type ◽  
Bilateral Carotid

✓ The effect of transient bilateral carotid occlusion on levels of free fatty acids, phospholipids, and lipid peroxides in the brain was studied in gerbils. During occlusion, both saturated and polyunsaturated free fatty acids increased strikingly to approximately 11-fold in total by 30 minutes. During recirculation, however, a selectively rapid decrement occurred in arachidonic acid, while saturated fatty acids gradually decreased to their basal levels in 180 minutes. The peroxide level, estimated by a thiobarbituric acid test, did not change during occlusion, but was elevated on reperfusion. Phosphatidylethanolamine content decreased throughout the periods examined. These results do not support a hypothesis that lipid peroxidation is initiated during ischemia by the lack of oxygen at the terminus of the mitochondrial respiratory chain. Instead, it is suggested that severe cerebral ischemia disintegrates membrane phospholipids, probably through activation of hydrolytic enzymes, and that overt peroxidative processes take place during reflow by means of restoration of oxygen supply. The peroxidative reactions may, indeed, cause additional damage during the postischemic phase.

Storage Quality of Brown Rice as Affected by Packaging with and without Carbon Dioxide

1980 ◽  
Vol 43 (12) ◽  
pp. 929-932 ◽  
Author(s):  
R. L. ORY ◽  
A. J. DELUCCA ◽  
A. J. ST. ANGELO ◽  
H. P. DUPUY
Keyword(s):  
Fatty Acids ◽  
Free Fatty Acids ◽  
Brown Rice ◽  
Lipid Peroxides ◽  
Ambient Temperatures ◽  
C Storage ◽  
Plastic Bags ◽  
End Use ◽  
Selection Of

Shelled brown rice (100 g/bag) was packed in regular plastic bags in air, in laminated film (nylon-EVA) bags in air, and in laminated bags plus CO2. Samples of each were stored in the dark at 4 C and at 24 C, and samples were removed after 1, 3, 5 and 7 months for analysis of odor changes, free fatty acids, total microbial counts, total lipolytic fungi and bacteria, lipid peroxides and gas chromatographic volatiles profiles. Brown rice in laminated bags plus CO2 was more stable under refrigerated conditions than at ambient temperatures. However, at 24-C storage there was no consistent significant decrease in free fatty acids, lipid peroxides and volatile compounds in these bags compared to the other types of packing. Laminated bags seem to have had an adverse effect on total microbial populations at both 4 and 24 C. Selection of either type of package for brown rice would be governed by end use, storage time and conditions.

Sign in / Sign up

Export Citation Format

Share Document