Lipid Peroxidation
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Diversity ◽  
2022 ◽  
Vol 14 (1) ◽  
pp. 55
Alyona Alexandrovna Nikonova ◽  
Sergey Mikhailovich Shishlyannikov ◽  
Nadezhda Antonovna Volokitina ◽  
Yuri Pavlovich Galachyants ◽  
Yuri Sergeevich Bukin ◽  

In this study, we present results on fatty acid analysis of phytoplankton of Lake Baikal, the world’s deepest lake, which differs from other lakes by its oceanic features. Since we used a large-mesh net, the net sample phytoplankton were primarily represented by the large elongated diatom Synedra acus. subsp. radians (Kützing) Skabichevskij. The similar algae composition of net samples of spring season phytoplankton collected at different sites of the lake allows us to compare results of the fatty acid analysis of these samples. The phytoplankton diversity of the sedimentation samples was contrary represented by 32 algae species. There are clear changes in the fatty acid composition of net phytoplankton exposed to anthropogenic impacts of varying intensity. The content of polyunsaturated fatty acids in phytoplankton collected from central stations (pelagic stations at a distance of ~10–30 km from the shoreline) without anthropogenic impact was higher by up to 15% than phytoplankton collected from nearshore stations (littoral stations at a distance of ~0.01–0.05 km from the shoreline) and offshore stations (pelagic stations at a distance of ~3 km from the shoreline). The interlaboratory precision of fatty acid determination of phytoplankton is estimated as ≤10%. We found high content of the lipid peroxidation marker (80–340 μg g−1 of dry weight) in phytoplankton from nearshore and offshore stations with intensive anthropogenic impact. In phytoplankton from central stations, we did not find any lipid peroxidation. Determination of unsaturated fatty acids, coupled with analysis of fatty acid peroxidation products, can be used to evaluate the level of anthropogenic impact in terms of ecological health and biodiversity conservation.

Science ◽  
2022 ◽  
Vol 375 (6577) ◽  
pp. 214-221
Marco Orecchioni ◽  
Kouji Kobiyama ◽  
Holger Winkels ◽  
Yanal Ghosheh ◽  
Sara McArdle ◽  

Sniffing out atherosclerosis Olfactory receptors are best known for their presence in the nose and their role in detecting smells, but they are also present in other tissues and perform additional biological functions. For example, vascular macrophages involved in the pathogenesis of atherosclerosis express multiple subtypes of olfactory receptors. Orecchioni et al . focused on olfactory receptor 2, a receptor for the compound octanal, and identified its contribution to atherosclerosis pathogenesis and the formation of atherosclerotic plaques (see the Perspective by Rayner and Rasheed). The authors show that most of the octanal was not directly derived from the diet, but rather was generated as a by-product of lipid peroxidation, suggesting a potential pathway for intervention. —YN

2022 ◽  
Vol 12 ◽  
Silvia Lucena Lage ◽  
Eduardo Pinheiro Amaral ◽  
Kerry L. Hilligan ◽  
Elizabeth Laidlaw ◽  
Adam Rupert ◽  

The poor outcome of the coronavirus disease-2019 (COVID-19), caused by SARS-CoV-2, is associated with systemic hyperinflammatory response and immunopathology. Although inflammasome and oxidative stress have independently been implicated in COVID-19, it is poorly understood whether these two pathways cooperatively contribute to disease severity. Herein, we found an enrichment of CD14highCD16− monocytes displaying inflammasome activation evidenced by caspase-1/ASC-speck formation in severe COVID-19 patients when compared to mild ones and healthy controls, respectively. Those cells also showed aberrant levels of mitochondrial superoxide and lipid peroxidation, both hallmarks of the oxidative stress response, which strongly correlated with caspase-1 activity. In addition, we found that NLRP3 inflammasome-derived IL-1β secretion by SARS-CoV-2-exposed monocytes in vitro was partially dependent on lipid peroxidation. Importantly, altered inflammasome and stress responses persisted after short-term patient recovery. Collectively, our findings suggest oxidative stress/NLRP3 signaling pathway as a potential target for host-directed therapy to mitigate early COVID-19 hyperinflammation and also its long-term outcomes.

2022 ◽  
Ning Liu ◽  
Zong Miao ◽  
Wei Tian ◽  
Zhongyuan Bao ◽  
Guangchi Sun ◽  

Abstract Background: Ferroptosis is a newly identified form of regulated cell death (RCD) characterized by the iron-dependent lipid reactive oxygen species (ROS) accumulation, but its exact mechanism in gliomas remains elusive. Acyl–coenzyme A (CoA) synthetase long-chain family member 4 (Acsl4), a pivotal enzyme in the regulation of lipid biosynthesis, has been found to benefit the initiation of ferroptosis, but its role in gliomas likewise needs clarification. Erastin, widely investigated as an inducer of ferroptosis, was recently found to regulate lipid peroxidation by regulating Acsl4 other than glutathione peroxidase 4 (GPX4) in ferroptosis. Methods: Relationship between Hsp90, Drp1 and Acsl4 was determined by Co-immunoprecipitation/ Mass spectrometry and western blot assay. The impact of Hsp90 and Drp1 on Acsl4-dependent ferroptosis was examined by lipid peroxidation indicators in patient-derived PL1 and PG7 cells. The morphological changes of mitochondria are observed by confocal-fluorescence microscopy and transmission electron microscope. Therapeutic efficacy of Erastin-induced ferroptosis in vivo was examined in xenograft mouse models.Results: In this study, we demonstrated that heat shock protein 90 (Hsp90) and dynamin-related protein 1 (Drp1) actively regulated Acsl4 expression in erastin-induced ferroptosis in gliomas. Hsp90 overexpression and calcineurin (CN)–mediated Drp1 dephosphorylation at serine 637 (Ser637) promoted ferroptosis by altering mitochondrial morphology and increasing Acsl4-mediated lipid peroxidation. Importantly, the Hsp90–Acsl4 pathway mediated Acsl4-dependent ferroptosis, amplifying the anticancer activity of erastin in vitro and in vivo. Conclusions: Our study not only uncovered an important role of Hsp90–Drp1–Acsl4 pathway in erastin-induced ferroptosis but also reveals an efficient mechanism of Acsl4 as a potential therapeutic target to ferroptosis-mediated glioma therapy.

Hai-Liang Zhang ◽  
Bing-Xin Hu ◽  
Zhi-Ling Li ◽  
Tian Du ◽  
Jia-Lu Shan ◽  

Lin Lin ◽  
Mu-Xin Zhang ◽  
Lei Zhang ◽  
Dan Zhang ◽  
Chao Li ◽  

Atherosclerosis is a chronic inflammatory disorder characterized by the gradual buildup of plaques within the vessel wall of middle-sized and large arteries. The occurrence and development of atherosclerosis and the rupture of plaques are related to the injury of vascular cells, including endothelial cells, smooth muscle cells, and macrophages. Autophagy is a subcellular process that plays an important role in the degradation of proteins and damaged organelles, and the autophagy disorder of vascular cells is closely related to atherosclerosis. Pyroptosis is a proinflammatory form of regulated cell death, while ferroptosis is a form of regulated nonapoptotic cell death involving overwhelming iron-dependent lipid peroxidation. Both of them exhibit distinct features from apoptosis, necrosis, and autophagy in morphology, biochemistry, and genetics. However, a growing body of evidence suggests that pyroptosis and ferroptosis interact with autophagy and participate in the development of cancers, degenerative brain diseases and cardiovascular diseases. This review updated the current understanding of autophagy, pyroptosis, and ferroptosis, finding potential links and their effects on atherogenesis and plaque stability, thus providing ways to develop new pharmacological strategies to address atherosclerosis and stabilize vulnerable, ruptured plaques.

Antioxidants ◽  
2022 ◽  
Vol 11 (1) ◽  
pp. 150
Marija Lesjak ◽  
Nataša Simin ◽  
Surjit K. S. Srai

Polyphenols, a diverse group of naturally occurring molecules commonly found in higher plants, have been heavily investigated over the last two decades due to their potent biological activities—among which the most important are their antioxidant, antimicrobial, anticancer, anti-inflammatory and neuroprotective activities. A common route of polyphenol intake in humans is through the diet. Since they are subjected to excessive metabolism in vivo it has been questioned whether their much-proven in vitro bioactivity could be translated to in vivo systems. Ferroptosis is a newly introduced, iron-dependent, regulated mode of oxidative cell death, characterized by increased lipid peroxidation and the accumulation of toxic lipid peroxides, which are considered to be toxic reactive oxygen species. There is a growing body of evidence that ferroptosis is involved in the development of almost all chronic diseases. Thus, ferroptosis is considered a new therapeutic target for offsetting many diseases, and researchers are putting great expectations on this field of research and medicine. The aim of this review is to critically analyse the potential of polyphenols to modulate ferroptosis and whether they can be considered promising compounds for the alleviation of chronic conditions.

2022 ◽  
Vol 11 (6) ◽  
pp. 716-724
Ahmed Benmahammed

Citrus fruits have long been qualified as veritable foods in view of the many therapeutic benefits they bring to the body. Several researchers have stud-ied the relationship between the bioactive compounds of Citrus and the health benefits and reduction of the risk of disease. Citrus sinensis, used in the food industry and its extracts have also been used in traditional medicine to activate vital energy, circulation, and weight loss, and appetite control. However, limited efforts have been made on collecting data on antioxidant potential of peels orange from the northern region of Algeria. Our study, therefore, focuses on the evaluation of total polyphenols compounds and in vitro assessment of their antioxidant potential of peels orange from the northern region of Algeria. The ethyl acetate and n-butanolic fractions from peels orange have been tested for their antioxidant activities and their lipid peroxidation inhibiting effects. The total phenolic and flavonoids content showed high levels. The preliminary phytochemical screening of tannins, phenolic compounds, flavonoids, coumarin, and alkaloids was also used. DPPH assay possesses strong potency to scavenge free radicals. The NO. radi-cal scavenging test exerts a good inhibitory effect. Furthermore, orange peels have been shown to suppress the lipid peroxidation of linoleic acid. Results further revealed a strong correlation between antioxidant effects and polyphenolic compounds. The high antioxidant activity of peel orange suggests that it could serve as a good natural antioxidant additive or food dietary supplement.

2022 ◽  
Vol 29 ◽  
Nadia Zaffaroni ◽  
Giovanni Luca Beretta

Abstract: Lipid peroxidation-driven iron-dependent ferroptosis is a regulated cell death mechanism implicated in numerous disease, such as neurological diseases, kidney injury, ischemia, and tumors, including prostate cancer. The cellular mechanisms of ferrosptosis are strongly associated with iron, reactive oxygen species and aminoacid metabolic pathways. Several compounds, namely ferroptosis inducers, impact on these pathways and trigger ferroptosis by i) inhibiting Xc– transporter system, ii) impairing GPX4 functions and iii) oxidizing iron and polyunsaturated phospholipids. Preclinical studies showed that in combination with conventional anticancer drugs, ferroptosis inducers are effective in prostate cancer and in combating the progression towards the castration resistant disease. This review overviews the mechanisms implicated in ferroptosis and discusses the findings achieved in prostate cancer.

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