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Nanotechnology-Mediated Radiation Therapy
Published in D. Sakthi Kumar, Aswathy Ravindran Girija, Bionanotechnology in Cancer, 2023
In the majority of the radiation-based cancer therapies, apoptosis takes the spotlight in causing cell death mechanisms; however, newer reports have started coming out to shift the focus toward whether cancer therapies can also induce other forms of cell death. In a study carried out by Lei G et al. demonstrated the link between ionizing radiation and a form of regulated cell death caused by lipid peroxidation called ferroptosis [58]. The authors analyzed that ionizing radiation in cancer cells led to the induction of reactive oxygen species (ROS) and upregulated expression of a lipid metabolizing enzyme ACSL4 to initiate ferroptosis. The study concluded that ferroptosis in cancer patients conferred better response and survival to radiotherapy.
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Published in Debasis Bagchi, Manashi Bagchi, Metal Toxicology Handbook, 2020
Amit Madeshiya, Pradipta Banerjee, Suman Santra, Nandini Ghosh, Sayantani Karmakar, Debasis Bagchi, Sashwati Roy, Amitava Das
Optimum levels of iron are necessary to maintain homeostasis, as deficiency or a high amount of iron leads to human diseases. Frey and Reed reported that in normal physiological condition, iron metabolism depends on (a) the actions of hormone, hepcidin, and iron exporter protein, ferroportin, and (b) iron regulatory proteins that bind iron-responsive elements [20]. When there is an iron overload, hydroxyl ions are produced which leads to oxidative stress in iron-sensitive tissues. Generation of ROS by iron-mediated pathway is an acute pathophysiological condition that may result in cell death in various organisms [21]. Iron-mediated cell death is often termed as ferroptosis.
Cellular and Molecular Toxicology of Nanoparticles
Published in Vladimir Torchilin, Handbook of Materials for Nanomedicine, 2020
A. Zielińska, D. Santos, J. R. Campos, A. Santini, P. Severino, A. A. M. Shimojo, S. B. Souto, E. B. Souto
Gaschler and Stockwell [32] also mentioned a non-apoptotic form of regulated cell death, which is dependent on iron and hence is known as ferroptosis. This process is characterized by the accumulation of lipid peroxides and can be attenuated by lipophilic antioxidants or iron chelators. Additionally, ferroptosis is not influenced by apoptosis or necroptosis inhibitors [32].
Experimental models of chemically induced Parkinson’s disease in zebrafish at the embryonic larval stage: a systematic review
Published in Journal of Toxicology and Environmental Health, Part B, 2023
Paola Briñez-Gallego, Dennis Guilherme da Costa Silva, Marcos Freitas Cordeiro, Ana Paula Horn, Mariana Appel Hort
The induction of oxidative stress was also determined for 6-OHDA. An increase in ROS production and MDA levels and a reduction in antioxidant defenses, including GSH levels, and activities of SOD, catalase (CAT), and GPx, were observed after exposure of zebrafish embryos and larvae to 6-OHDA (Li et al. 2018; Sun et al. 2020; Wu et al. 2021). 6-OHDA also enhanced Keap1, a repressor of Nrf-2, reducing activation of this transcription factor and consequently leading to a decrease in enzymes regulated by the Nrf2-ARE signaling pathway: HO-1, GCLC, GCLM, and nicotinamide adenine dinucleotide phosphate quinone dehydrogenase (NQO1) (Li et al. 2018; Wu et al. 2021). Sun et al. (2020) investigated whether 6-OHDA induced ferroptosis, which is recognized as a form of cell death that involves the breakdown of the antioxidant defense system, depletion of GSH, and lipid peroxidation induced by iron (Dixon et al. 2012). Sun et al. (2020) found that ferroptosis was elevated in embryos and larvae exposed to 6-OHDA, a condition that may be one of the causes of neuronal death.
A review of microalgal cell wall composition and degradation to enhance the recovery of biomolecules for biofuel production
Published in Biofuels, 2023
Syafiqah Md Nadzir, Norjan Yusof, Norazela Nordin, Azlan Kamari, Mohd Zulkhairi Mohd Yusoff
In contrast, paraptosis is a non-apoptotic form of PCD accompanied by endoplasmic reticulum and mitochondrial dilation, chromatin spotting without DNA fragmentation, significant cytoplasmic swelling and vacuolation, and alternative caspase activation [127]. It is mediated by mitogen-activated protein kinases and differs significantly from apoptosis due to the absence of caspase activity [128]. Another non-apoptotic form of PCD, depending on the presence of iron, is ferroptosis. It is associated with lipid peroxidation and accumulation of ROS [129]. Iron molecules induce harmful lipid accumulation by ROS, which is mediated by inhibition of cysteine import and glutathione depletion [130]. Autophagy, in contrast, is a type of PCD marked by a rise in the number of autophagosomes, autolysosomes, and small lytic vacuoles. It is a catabolic process induced by the autophagy gene (atg) that degrades long-lived organelles and proteins. Autophagy can be used to selectively degrade organelles such as mitochondria (mitophagy) and ribosomes (ribophagy), as well as misfolded and aggregated proteins [131,132]. The early stage of autophagy consists of the induction and formation of autophagosomes, whereas the late stage includes the fusion of autophagosomes and lysosomes, followed by degradation of the fusion complex and reformation of lysosomes [133].
Ex vivo treatment with fucoidan of mononuclear cells from SARS-CoV-2 infected patients
Published in International Journal of Environmental Health Research, 2022
K. J. G. Díaz-Resendiz, G. A. Toledo-Ibarra, R. Ruiz-Manzano, D.A. Giron Perez, C.E. Covantes-Rosales, A. B. Benitez-Trinidad, K. M Ramirez-Ibarra, A. T. Hermosillo Escobedo, I. González-Navarro, G.H. Ventura-Ramón, A. Romero Castro, D. Alam Escamilla, A. Y. Bueno-Duran, Manuel Iván Girón-Pérez
Ferroptosis is a mechanism of non-apoptotic programmed cell death, which is caused by inhibition of the Xc-Cys/Glu system that does not allow intracellular iron chelation by increased ROS production through glutathione (GSH) inhibition and loss of GPX4 function, leading to oxidative stress, lipid peroxidation, Ca2+ influx and cell death (Cao and Dixon 2016; Fearnhead et al. 2017; Lei et al. 2019). In this context, fucoidan treatment has been reported to reduce oxidative stress by inducing an increase in the activity of antioxidant enzymes such as GSH, GPx, SOD and CAT (Hong et al. 2012; Boshy et al. 2017; AlKahtane et al. 2020; Abdel-Daim et al. 2020). Thus, the results of the present investigation suggest that fucoidan may act as an antioxidant treatment (intracellularly regulating free iron levels) counteracting the oxidative stress caused by mitochondrial dysfunction of PBMCs in women recovered from SARS-CoV-2 (Figure 6).