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Samantha W Alvarez, Richard Possemato
No abstract text is available yet for this article.
February 16, 2018: Oncotarget
Naho Hirayama, Toshihiko Aki, Takeshi Funakoshi, Kanako Noritake, Kana Unuma, Koichi Uemura
Paraquat (PQ) is an herbicide that was once used worldwide, but is now prohibited in many nations due to its high toxicity to humans. However, there are still rare cases of the fetal intoxication of PQ, which was purchased prior to the prohibition in Japan. In this study, several cell death pathways, the mitochondrial stress response, and autophagy were examined in SH-SY5Y cells exposed to PQ. The results reveal the decrease of a mitochondrial stress sensitive-BNIP3 (Bcl-2/adenovirus E1B 19-kDa-interacting protein 3) protein, the suppression of autophagic flux, and the lack of apoptosis as well as other regulated forms of necrosis, such as necroptosis and ferroptosis...
2018: Journal of Toxicological Sciences
Jose Pedro Friedmann Angeli, Marcus Conrad
Selenium has transitioned from an environmental poison and carcinogen to an essential micronutrient associated with a broad array of health promoting effects. These beneficial effects are now accepted to be linked to its incorporation into selenoproteins, a family of rare proteins utilizing a specialized translation machinery to integrate selenium in the form of selenocysteine. Despite this recognised role, much less is known regarding the actual role of selenium in these proteins. Here, we will provide the reader with an overview of the essential role of specific selenoproteins and their link to pathology based on mouse studies and relevant mutations discovered in humans...
March 6, 2018: Free Radical Biology & Medicine
Michael M Gaschler, Fanghao Hu, Huizhong Feng, Andreas Linkermann, Wei Min, Brent R Stockwell
Ferroptosis is a form of non-apoptotic cell death characterized by the unchecked accumulation of lipid peroxides. Ferrostatin-1 and its analogs (ferrostatins) specifically prevent ferroptosis in multiple contexts, but many aspects of their molecular mechanism of action remain poorly described. Here, we employed stimulated Raman scattering (SRS) microscopy coupled with small vibrational tags to image the distribution of ferrostatins in cells, and found that they accumulate in lysosomes, mitochondria, and endoplasmic reticulum...
March 7, 2018: ACS Chemical Biology
Chloé Sauzay, Christophe Louandre, Sandra Bodeau, Frédéric Anglade, Corinne Godin, Zuzana Saidak, Jean-Xavier Fontaine, Cédric Usureau, Nathalie Martin, Roland Molinie, Julie Pascal, François Mesnard, Olivier Pluquet, Antoine Galmiche
Sorafenib is the first line treatment for advanced hepatocellular carcinoma (HCC). We explored its impact on the proteostasis of cancer cells, i.e. the processes that regulate the synthesis, maturation and turn-over of cellular proteins. We observed that sorafenib inhibits the production of the tumour marker alpha-foetoprotein (AFP) in two different HCC cell lines, an effect that correlated with a radical inhibition of protein biosynthesis. This effect was observed at clinically relevant concentrations of sorafenib and was not related to the effect of sorafenib on the transport of amino acids across the plasma membrane or the induction of the unfolded protein response (UPR)...
February 2, 2018: Oncotarget
Michael Fricker, Aviva M Tolkovsky, Vilmante Borutaite, Michael Coleman, Guy C Brown
Neuronal cell death occurs extensively during development and pathology, where it is especially important because of the limited capacity of adult neurons to proliferate or be replaced. The concept of cell death used to be simple as there were just two or three types, so we just had to work out which type was involved in our particular pathology and then block it. However, we now know that there are at least a dozen ways for neurons to die, that blocking a particular mechanism of cell death may not prevent the cell from dying, and that non-neuronal cells also contribute to neuronal death...
April 1, 2018: Physiological Reviews
Maysa Sarhan, Walter G Land, Wulf Tonnus, Christian P Hugo, Andreas Linkermann
When cells undergo necrotic cell death in either physiological or pathophysiological settings in vivo, they release highly immunogenic intracellular molecules and organelles into the interstitium and thereby represent the strongest known trigger of the immune system. With our increasing understanding of necrosis as a regulated and genetically determined process (RN, regulated necrosis), necrosis and necroinflammation can be pharmacologically prevented. This review discusses our current knowledge about signaling pathways of necrotic cell death as the origin of necroinflammation...
April 1, 2018: Physiological Reviews
Yuko Kinowaki, Morito Kurata, Sachiko Ishibashi, Masumi Ikeda, Anna Tatsuzawa, Masahide Yamamoto, Osamu Miura, Masanobu Kitagawa, Kouhei Yamamoto
Regulation of oxidative stress and redox systems has important roles in carcinogenesis and cancer progression, and for this reason has attracted much attention as a new area of cancer therapeutic targets. Glutathione peroxidase 4 (GPX4), an antioxidant enzyme, has biological important functions such as signaling cell death by suppressing peroxidation of membrane phospholipids. However, few studies exist on the expression and clinical relevance of GPX4 in malignant lymphomas such as diffuse large B-cell lymphoma...
February 20, 2018: Laboratory Investigation; a Journal of Technical Methods and Pathology
Jiraporn Ousingsawat, Podchanart Wanitchakool, Rainer Schreiber, Karl Kunzelmann
Pyroptosis is a highly inflammatory form of programmed cell death that is caused by infection with intracellular pathogens and activation of canonical or noncanonical inflammasomes. The purinergic receptor P2X7 is activated by the noncanonical inflammasome and contributes essentially to pyroptotic cell death. The Ca2+ activated phospholipid scramblase and ion channel TMEM16F has been shown earlier to control cellular effects downstream of purinergic P2X7 receptors that ultimately lead to cell death. As pyroptotic cell death is accompanied by an increases in intracellular Ca2+ , we asked whether TMEM16F is activated during pyroptosis...
February 20, 2018: Cell Death & Disease
Ron Mittler, Merav Darash-Yahana, Yang Sung Sohn, Fang Bai, Luhua Song, Ioav Zvi Cabantchik, Patricia Jennings, Jose Onuchic, Rachel Nechushtai
SIGNIFICANCE: Cancer cells accumulate high levels of iron and reactive oxygen species (ROS) to promote their high metabolic activity and proliferation rate. However, high levels of iron and ROS can also lead to enhanced oxidative stress and the activation of cell death pathways such as apoptosis and ferroptosis. This has led to the proposal that different drugs that target iron and/or ROS metabolism could be used as anticancer drugs. However, due to the complex role iron and ROS play in cells, the majority of these drugs yielded mixed results, highlighting a critical need to identify new players in the regulation of iron and ROS homeostasis in cancer cells...
February 20, 2018: Antioxidants & Redox Signaling
Markus Griesser, Ron Shah, Antonius T Van Kessel, Omkar Zilka, Evan A Haidasz, Derek A Pratt
Sterically-hindered nitroxides such as 2,2,6,6-tetramethylpiperidin-N-oxyl (TEMPO) have long been ascribed antioxidant activity that is thought to underlie their chemopreventive and anti-aging properties. However, the most commonly invoked reactions in this context - combination with an alkyl radical to give a redox inactive alkoxyamine or the catalysis of superoxide dismutation - are unlikely to be relevant under (most) physiological conditions. Herein we characterize the kinetics and mechanisms of the reactions of TEMPO, as well as an N-arylnitroxide and a N,N-diarylnitroxide, with alkylperoxyl radicals, the propagating species in lipid peroxidation...
February 16, 2018: Journal of the American Chemical Society
Li Li, Yu Hao, Yu Zhao, Huijuan Wang, Xiujun Zhao, Yan Jiang, Fulu Gao
Sertoli cell death contributes to spermatogenesis impairment, which is associated with male infertility. Testicular ischemia‑reperfusion (I/R) injury induces the cell death of germ cells and Sertoli cells, whereas inhibition of cell death ameliorates acute testicular I/R damage. The aim of the present study was to investigate the mechanism of I/R stress-induced cell death in TM4 cells. Oxygen‑glucose deprivation and reoxygenation (OGD/R) was demonstrated to induce I/R injury and cell death in TM4 cells...
February 7, 2018: International Journal of Molecular Medicine
Bei Liu, Chunxia Zhao, Hongkun Li, Xiaoqian Chen, Yu Ding, Sudan Xu
Heart failure (HF) is the end stage of cardiovascular disease and is characterized by the loss of myocytes caused by cell death. Puerarin has been found to improve HF clinically, and animal study findings have confirmed its anti-cell-death properties. However, the underlying mechanisms remain unclear, especially with respect to the impact on ferroptosis, a newly defined mechanism of iron-dependent non-apoptotic cell death in HF. Here, ferroptosis-like cell death was observed in erastin- or isoprenaline (ISO)-treated H9c2 myocytes in vitro and in rats with aortic banding inducing HF, characterized by reduced cell viability with increased lipid peroxidation and labile iron pool...
February 7, 2018: Biochemical and Biophysical Research Communications
Hong Zhu, Aijun Sun
Programmed cell death plays an essential role in myocardial homeostasis and pathology. Three distinct forms of programmed cell death have been identified, namely apoptosis, necrosis, and autophagic cell death. Necrosis, previously known as an unregulated form of cell death, has been recognized as a highly regulated process now and attracted great attention over the past decade. Programmed necrosis mainly refers to necroptosis, pyroptosis, ferroptosis, and mitochondrial permeability transition (MPT)-dependent necrosis...
March 2018: Journal of Molecular and Cellular Cardiology
Sara R Fedorka, Kevin So, Ayad A Al-Hamashi, Ibtissam Gad, Ronit Shah, Veronika Kholodovych, Hanan D Alqahtani, William R Taylor, L M Viranga Tillekeratne
In the course of generating a library of open-chain epothilones, we discovered a new class of small molecule anticancer agents that has no effect on tubulin but instead kills selected cancer cell lines by harnessing reactive oxygen species in an iron-dependent manner. Results of the preliminary studies are consistent with the recently described cell death mechanism ferroptosis. Studies are in progress to confirm ferroptosis as the cell death mechanism and to identify the specific molecular targets of these small molecule anticancer agents...
February 7, 2018: Organic & Biomolecular Chemistry
Jing Ye, Ruonan Zhang, Fan Wu, Lijuan Zhai, Kaifeng Wang, Mang Xiao, Tian Xie, Xinbing Sui
Traditional cancer therapy is mainly targeting on enhancing cell apoptosis, however, it is well established that many cancer cells are chemo-resistant and defective in apoptosis induction. Therefore, it may have important therapeutic implications to exploit some novel natural compounds based on non-apoptotic programmed cell death. Currently, accumulating evidence shows that the compounds from nature source can induce non-apoptotic programmed cell death in cancer cells, and therefore these natural compounds have gained a great promise for the future anticancer therapeutics...
January 30, 2018: Cancer Letters
Harshal Nemade, Umesh Chaudhari, Aviseka Acharya, Jürgen Hescheler, Jan Georg Hengstler, Symeon Papadopoulos, Agapios Sachinidis
Etoposide (ETP) and anthracyclines are applied for wide anti-cancer treatments. However, the ETP-induced cardiotoxicity remains to be a major safety issue and the underlying cardiotoxic mechanisms are not well understood. This study is aiming to unravel the cardiotoxicity profile of ETP in comparison to anthracyclines using physiologically relevant human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs). Using xCELLigence real-time cell analyser (RTCA), we found that single high dose of ETP induces irreversible increase in hPSC-CMs beating rate and decrease in beating amplitude...
February 3, 2018: Archives of Toxicology
Frank Thévenod
Iron (Fe) is an essential metal, vital for biological functions, including electron transport, DNA synthesis, detoxification, and erythropoiesis that all contribute to metabolism, cell growth, and proliferation. Interactions between Fe and O2 can result in the generation of reactive oxygen species (ROS), which is based on the ability of Fe to redox cycle. Excess Fe may cause oxidative damage with ensuing cell death, but DNA damage may also lead to permanent mutations. Hence Fe is carcinogenic and may initiate tumor formation and growth, and also nurture the tumor microenvironment and metastasis...
February 5, 2018: Metal Ions in Life Sciences
Yuki Yamaguchi, Takashi Kasukabe, Shunichi Kumakura
Pancreatic cancer is one of the most lethal types of cancer with a mortality rate of almost 95%. Treatment with current chemotherapeutic drugs has limited success due to poor responses. Therefore, the development of novel drugs or effective combination therapies is urgently required. Piperlongumine (PL) is a natural product with cytotoxic properties restricted to cancer cells by significantly increasing intracellular reactive oxygen species (ROS) levels. In the present study, we demonstrated that PL induced cancer cell death through, at least in part, the induction of ferroptosis, as the cancer cell-killing activity was inhibited by the antioxidant, N‑acetylcysteine, ferroptosis inhibitors (ferrostatin‑1 and liproxstatin‑1) and the iron chelator, deferoxamine (DFO), but not by the apoptosis inhibitor, Z-VAD-FMK, or the necrosis inhibitor, necrostatin‑1...
January 31, 2018: International Journal of Oncology
Se Hoon Hong, Dae-Hee Lee, Young-Sun Lee, Min Jee Jo, Yoon A Jeong, William T Kwon, Haroon A Choudry, David L Bartlett, Yong J Lee
Ferroptosis is a type of programmed cell death that depends on iron and is characterized by the accumulation of lipid peroxides. In the present study, we investigated the nature of the interplay between ferroptosis and other forms of cell death such as apoptosis. Human pancreatic cancer PANC-1 and BxPC-3 and human colorectal cancer HCT116 cells were treated with ferroptotic agents such as erastin and artesunate (ART) in combination with the apoptotic agent tumor necrosis factor-related apoptosis-inducing ligand (TRAIL)...
December 29, 2017: Oncotarget
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