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Yan Zhang, Chao Sun, Chenxi Zhao, Jian Hao, Yiling Zhang, Baoyou Fan, Bo Li, Huiquan Duan, Chang Liu, Xiaohong Kong, Ping Wu, Xue Yao, Shiqing Feng
Cell death is a key issue in spinal cord secondary injury. Ferroptosis is recently discovered as an iron-dependent type of cell death that is distinct from other forms of cell death pathways such as apoptosis and necrosis. This research is aimed to investigate the role of ferroptosis in spinal cord injury (SCI) pathophysiology, and to explore the effectiveness of ferroptosis inhibitor on SCI. We examined the ferroptosis markers and the factors in a rat contusion SCI model. Seen from transmission electron microscopy (TEM) following SCI, mitochondria showed ferroptotic characteristic changes...
October 20, 2018: Brain Research
Daiha Shin, Eun Hye Kim, Jaewang Lee, Jong-Lyel Roh
Glutathione peroxidase 4 (GPX4) is a regulator of ferroptosis (iron-dependent, non-apoptotic cell death); its inhibition can render therapy-resistant cancer cells susceptible to ferroptosis. However, some cancer cells develop mechanisms protective against ferroptosis; understanding these mechanisms could help overcome chemoresistance. In this study, we investigated the molecular mechanisms underlying resistance to ferroptosis induced by GPX4 inhibition in head and neck cancer (HNC). The effects of two GPX4 inhibitors, (1S, 3R)-RSL3 and ML-162, and of trigonelline were tested in HNC cell lines, including cisplatin-resistant (HN3R) and acquired RSL3-resistant (HN3-rslR) cells...
October 16, 2018: Free Radical Biology & Medicine
Cong Li, Xiaobing Deng, Xiaowen Xie, Ying Liu, José Pedro Friedmann Angeli, Luhua Lai
The anti-oxidative enzyme, glutathione peroxidase 4 (GPX4), helps to promote inflammation resolution by eliminating oxidative species produced by the arachidonic acid (AA) metabolic network. Up-regulating its activity has been proposed as a promising strategy for inflammation intervention. In the present study, we aimed to study the effect of GPX4 activator on the AA metabolic network and inflammation related pathways. Using combined computational and experimental screen, we identified a novel compound that can activate the enzyme activity of GPX4 by more than two folds...
2018: Frontiers in Pharmacology
Jung Min Kim, Hyeong Geug Kim, Chang Gue Son
Oxidative stress is a common phenomenon and is linked to a wide range of diseases and pathological processes including aging. Tissue-specific variation in redox signaling and cellular responses to oxidative stress may be associated with vulnerability especially to age-related and chronic diseases. In order to provide a basis for tissue-specific difference, we examined the tissue-specific transcriptional features of 101 oxidative stress-associated genes in 10 different tissues and organs of healthy mice under physiological conditions...
October 15, 2018: International Journal of Molecular Sciences
Yun-Wei Pang, Xiao-Long Jiang, Ya-Chun Wang, Yang-Yang Wang, Hai-Sheng Hao, Shan-Jiang Zhao, Wei-Hua Du, Xue-Ming Zhao, Lin Wang, Hua-Bin Zhu
Paraquat (PQ), a broad-spectrum agricultural pesticide, causes cellular toxicity by increasing oxidative stress levels in various biological systems, including the reproductive system. PQ exposure causes embryotoxicity and reduces the developmental abilities of embryos. However, there is little information regarding the toxic effects of PQ on oocyte maturation. In this study, we studied the toxic effects of PQ exposure and the effects of melatonin on PQ-induced damage in bovine oocytes. PQ exposure disrupted nuclear and cytoplasmic maturation, which was manifested as decreased cumulus cell expansion, reduced first polar body extrusion, and abnormal distribution patterns of cortical granules and mitochondria...
October 15, 2018: Journal of Pineal Research
Eitezaz Mahmood, Jelliffe Jeganathan, Ruby Feng, Maria Saraf, Kamal Khabbaz, Faraz Mahmood, Senthilnathan Venkatachalam, David Liu, Louis Chu, Samir M Parikh, Robina Matyal
BACKGROUND: The mechanism of mitochondrial dysfunction following cardiopulmonary bypass (CPB) in diabetics lacks understanding. We hypothesized that impaired beta-oxidation of fatty acids leads to worsened stress response in this patient population after cardiac surgery. METHODS: After IRB approval, right atrial tissue samples were collected from 35 diabetic and 33 non-diabetics pre- and post-CPB. Patients with HbA1c ≥ 6.0 and a clinical diagnosis of diabetes mellitus were considered to be diabetic...
October 3, 2018: Annals of Thoracic Surgery
Che-Lin Hu, Mara Nydes, Kara L Shanley, Itzy E Morales Pantoja, Tamara A Howard, Oscar A Bizzozero
Glutathione peroxidase 4 (GPx4) is the only enzyme capable of reducing toxic lipid hydroperoxides in biological membranes to the corresponding alcohols using GSH as the electron donor. GPx4 is the major inhibitor of ferroptosis, a non-apoptotic and iron-dependent programmed cell death pathway, which has been shown to occur in various neurological disorders with severe oxidative stress. In this study, we investigate whether GPx4 expression is altered in multiple sclerosis (MS) and its animal model experimental autoimmune encephalomyelitis (EAE)...
October 5, 2018: Journal of Neurochemistry
Jianli Xue, Zixin Min, Zhuqing Xia, Bin Cheng, Binshang Lan, Fujun Zhang, Yan Han, Kunzheng Wang, Jian Sun
BACKGROUND: The phenotypes of osteoarthritis (OA) consist of cartilage extracellular matrix (ECM) metabolism disorder and the breakdown of cartilage homeostasis, which are induced by pro-inflammatory factors and oxidative stress. Selenoproteins regulated by selenocysteine insertion sequence binding protein 2 (SBP2) are highly effective antioxidants, but their regulatory mechanisms, particularly the involvement of miRNAs, are not fully understood. METHODS: To explore whether miR-181a-5p and SBP2 are involved in OA pathogenesis, we established an IL-1β model using the chondrocyte SW1353 cell line...
October 5, 2018: BMC Musculoskeletal Disorders
E C Dos Santos, R Varchetta, C B de Lima, J Ispada, H S Martinho, P K Fontes, M F G Nogueira, B Gasparrini, M P Milazzotto
The earliest stages of embryo development are deeply influenced by reactive oxygen species (ROS), byproducts of the mitochondrial oxygen metabolism that play a key role as messengers in normal cell signal transduction and cell cycling. Despite its positive roles, the imbalance caused by the excess of ROS and an inefficient antioxidant system leads to oxidative stress, with negative consequences to the cell such as DNA damage, metabolic changes, mitochondrial stress and cell death. In the present work, crocetin - a natural antioxidant - was added to the culture media of bovine embryos to evaluate the efficiency of its antioxidant capability during embryo culture...
January 1, 2019: Theriogenology
Zixin Min, Yuanxu Guo, Mengyao Sun, Safdar Hussain, Yitong Zhao, Dongxian Guo, Huang Huang, Lisong Heng, Fujun Zhang, Qilan Ning, Yan Han, Peng Xu, Nannan Zhong, Jian Sun, Shemin Lu
Selenium (Se) deficiency brings about defects in the biosynthesis of several selenoproteins and has been associated with aberrant chondrogenesis. Selenocysteine (Sec) Insertion Sequence (SECIS) and SECIS binding protein 2 (SBP2) interaction is a very critical node for the metabolic balance between Se and selenoproteins. The Gpx1, Gpx4 and SelS have different binding affinities with SBP2 in cells. According to our results, both miR-181a-5p and SBP2 appeared to be selenium-sensitive and regulated the expression of selenoproteins in C28/I2 cells under Se sufficient environment...
December 2018: Journal of Cellular and Molecular Medicine
Tiantian Meng, Yi-Lin Liu, Chun-Yan Xie, Bin Zhang, Yi-Qiang Huang, Ya-Wei Zhang, Yajun Yao, Ruilin Huang, Xin Wu
Supplementation of selenium (Se) is a common practice in the poultry industry via sodium selenite (SS) and selenium yeast (SY), while the effects of nano-selenium (NS) on laying hens are poorly known. This study aimed to compare the effects of NS, SS, and SY on productivity; selenium (Se) deposition in eggs; and antioxidant capacity in laying hens. A total of 288 30-week-old Brown Hy-line laying hens were randomly assigned into four dietary treatments, which included corn-soybean meal basal diet (Con) without Se sources and basal diets supplemented with 0...
September 19, 2018: Biological Trace Element Research
Tobias M Seibt, Bettina Proneth, Marcus Conrad
Ferroptosis is a non-apoptotic form of cell death characterized by iron-dependent lipid peroxidation and metabolic constraints. Dependence on NADPH/H+, polyunsaturated fatty acid metabolism, and the mevalonate and glutaminolysis metabolic pathways have been implicated in this novel form of regulated necrotic cell death. Genetic studies performed in cells and mice established the selenoenzyme glutathione peroxidase (GPX4) as the key regulator of this form of cell death. Besides these genetic models, the identification of a series of small molecule ferroptosis-specific inhibitors and inducers have not only helped in the delineation of the molecular underpinnings of ferroptosis but they might also prove highly beneficial when tipping the balance between cell death inhibition and induction in the context of degenerative diseases and cancer, respectively...
September 13, 2018: Free Radical Biology & Medicine
D A Stoyanovsky, Y Y Tyurina, I Shrivastava, I Bahar, V A Tyurin, O Protchenko, S Jadhav, S B Bolevich, A V Kozlov, Y A Vladimirov, A A Shvedova, C C Philpott, H Bayir, V E Kagan
Duality of iron as an essential cofactor of many enzymatic metabolic processes and as a catalyst of poorly controlled redox-cycling reactions defines its possible biological beneficial and hazardous role in the body. In this review, we discuss these two "faces" of iron in a newly conceptualized program of regulated cell death, ferroptosis. Ferroptosis is a genetically programmed iron-dependent form of regulated cell death driven by enhanced lipid peroxidation and insufficient capacity of thiol-dependent mechanisms (glutathione peroxidase 4, GPX4) to eliminate hydroperoxy-lipids...
September 12, 2018: Free Radical Biology & Medicine
Kui Liu, Meng Jin, Li Xiao, Huiguo Liu, Shuang Wei
Introduction: Glutathione peroxidases (GPxs) constitutes an enzyme family which has the ability to reduce free hydrogen peroxide to water and lipid hydroperoxides to their corresponding alcohols, and its main biological roles are to protect organisms from oxidative stress-induced damage. GPxs include eight members in different tissues of the body, and they play essential roles in carcinogenesis. However, the prognostic value of individual GPx in non-small cell lung cancer (NSCLC) remains elusive...
2018: Cancer Management and Research
A Arangasamy, Renu Balkrishan Sharma, K Hemalatha, M Venkata Krishnaiah, S Selvaraju, G Pushpa Rani, B K Binsila, N M Soren, I J Reddy, J P Ravindra, Raghavendra Bhatta
The antioxidant properties and the protective role of organic zinc (Zn) and copper (Cu) in white blood cells (WBCs) and spermatozoa were analyzed through quantification of superoxide dismutase 1 (SOD1), catalase (CAT), glutathione peroxidase 4 (GPx4) and nuclear factor erythroid 2-like 2 (NFE2L2) and correlations were determined with sperm functional characteristics in Osmanabadi bucks. Bucks (aged 5 months; n = 40) were divided into ten groups, and the dietary treatments comprised of a control and nine treatment groups as follows: organic Zn as Zn 20, Zn 40 and Zn 60, organic Cu as Cu 12...
October 2018: Animal Reproduction Science
Ewa Strauss, Jolanta Tomczak, Ryszard Staniszewski, Grzegorz Oszkinis
BACKGROUND: Little is known on the role of selenoprotein genes in cardiovascular disease. This study examines the associations of the SEPP1, SELENOS, TXNRD1, TXNRD2, GPX4, and SOD2 polymorphisms and selenoprotein P (SeP) and thioredoxin concentrations with the development of abdominal aortic aneurysm (AAA) and aortoiliac occlusive disease (AOID), as well as their influence on cardiac phenotype. METHODS: 564 patients with AAA, 400 patients with AIOD, and 543 controls were enrolled and characterized for coronary artery disease, myocardial infarction, and systolic heart failure (HF) occurrence...
2018: PloS One
Csilla Pelyhe, Benjámin Kövesi, Erika Zándoki, Balázs Kovács, Márta Erdélyi, Szabina Kulcsár, Miklós Mézes, Krisztián Balogh
Co-occurrence of mycotoxin contamination of feeds is a frequent problem, therefore the purpose of this study was to evaluate the combined effect of T-2 toxin and deoxynivalenol (DON) on lipid peroxidation, parameters and regulation of the glutathione redox system in broiler chickens in a sub-chronic (7 day) study. The applied doses were: low mix: 0.23 mg T-2 toxin and 4.96 mg DON/kg feed; medium mix: 1.21 mg T-2 toxin and 12.38 mg DON/kg feed; and high mix: 2.42 T-2 toxin and 24.86 mg DON/kg feed...
October 2018: Toxicon: Official Journal of the International Society on Toxinology
Jia-Rui Wu, Qing-Zhang Tuo, Peng Lei
Ferroptosis is a recently defined form of cell death with the involvement of iron and reactive oxygen species (ROS), which is distinct from apoptosis, autophagy and other forms of cell death. Emerging evidence suggested that iron accumulation and lipid peroxidation can be discovered in various neurological diseases, accompanied with reduction of glutathione (GSH) and glutathione peroxidase 4 (GPX4). In addition, ferroptotic inhibitors have been shown to protect neurons, and recover the cognitive function in disease animal models...
October 2018: Journal of Molecular Neuroscience: MN
Bettina Proneth, Marcus Conrad
Ferroptosis is a non-apoptotic form of cell death characterized by overwhelming iron-dependent lipid peroxidation, which contributes to a number of pathologies, most notably tissue ischemia/reperfusion injury, neurodegeneration and cancer. Cysteine availability, glutathione biosynthesis, polyunsaturated fatty acid metabolism and modulation of the phospholipidome are the key events of this necrotic cell death pathway. Non-enzymatic and enzymatic lipoxygenase (LOX)-mediated lipid peroxidation of lipid bilayers is efficiently counteracted by the glutathione (GSH)/glutathione peroxidase 4 (GPX4) axis...
August 6, 2018: Cell Death and Differentiation
Tine Iskov Kopp, Malene Outzen, Anja Olsen, Ulla Vogel, Gitte Ravn-Haren
Background: Selenium is an essential trace element and is suggested to play a role in the etiology of a number of chronic diseases. Genetic variation in genes encoding selenoproteins, such as selenoprotein P and the glutathione peroxidases, may affect selenium status and, thus, individual susceptibility to some chronic diseases. In the present study, we aimed to (1) investigate the effect of mussel and fish intake on glutathione peroxidase enzyme activity and (2) examine whether single nucleotide polymorphisms in the GPX1 , GPX4 , and SELENOP genes modify the effect of mussel and fish intake for 26 weeks on whole blood selenium, plasma selenoprotein P concentrations, and erythrocyte GPX enzyme activity in a randomized intervention trial in Denmark...
2018: Genes & Nutrition
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