Inhibitors against cystine-glutamate antiporter, including erastin, elicit ferroptotic cell death. The erastin-induced ferroptotic cell death appears to be caused by cysteine as well as glutathione depletion. Cysteine is an essential substrate for sulfane sulfur producing systems in cells, generating persulfides that function as intracellular antioxidants and intermediates in iron-sulfur cluster production. Therefore, we examined whether botanical sulfane sulfur donors such as diallyl trisulfide (DATS) and dimethyl trisulfide (DMTS) prevent ferroptotic cell death in HT1080 cells treated with erastin. As a result, DMTS (20 μM) and DATS (10 μM) rescued the erastin-treated HT1080 cells by 69.6% and 91.6%, respectively. Furthermore, DMTS-containing squeeze of cabbage (2.0 g/L) and DATS-containing squeeze of garlic (0.07 g/L) rescued the erastin-treated HT1080 cells by 76.5% and almost 100%, respectively. In conclusion, the ingestion of trisulfides may bring about increased resistance to ferroptotic cell death in vivo.
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http://dx.doi.org/10.1016/j.foodchem.2020.128511 | DOI Listing |
Int J Pharm X
June 2025
Department of Gynecology, The Affiliated Hospital of Kunming University of Science and Technology, The First People's Hospital of Yunnan Province, Kunming, PR China.
As a recently discovered form of regulated cell death, ferroptosis has attracted much attention in the field cancer therapy. However, achieving considerably enhanced efficacy is often restricted by the overexpression of endogenous glutathione (GSH) in tumor microenvironment (TME). In this work, we report a ferroptosis-inducing strategy of GSH depletion and reactive oxygen species (ROS) generation based on a biodegradable copper-doped calcium phosphate (CaP) with L-buthionine sulfoximine (BSO) loading (denoted as BSO@CuCaP-LOD, BCCL).
View Article and Find Full Text PDFBiochem Biophys Rep
March 2025
Orthopedics of TCM Senior Department, The Sixth Medical Center of PLA General Hospital, Beijing, 100048, China.
Background: Intervertebral disc degeneration (IVDD) has been linked to ferroptosis, a type of programmed cell death. The role of platelet-rich plasma (PRP) in mitigating ferroptosis in nucleus pulposus (NP) cells within IVDD remains unclear.
Purpose: This study aims to verify the effectiveness of PRP in reducing ferroptosis in NP cells induced by Erastin.
Neurobiol Dis
January 2025
Center for Translational Research in Neurodegenerative Disease, College of Medicine, University of Florida, Gainesville, FL, USA; Department of Neuroscience, College of Medicine, University of Florida, Gainesville, FL, USA; McKnight Brain Institute, University of Florida, Gainesville, FL, USA; Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, USA; Norman Fixel Institute for Neurological Diseases, University of Florida, Gainesville, FL, USA. Electronic address:
Parkinson's Disease (PD) is a multisystem disorder in which dysregulated neuroimmune crosstalk and inflammatory relay via the gut-blood-brain axis have been implicated in PD pathogenesis. Although alterations in circulating inflammatory cytokines and reactive oxygen species (ROS) have been associated with PD, no biomarkers have been identified that predict clinical progression or disease outcome. Gastrointestinal (GI) dysfunction, which involves perturbation of the underlying immune system, is an early and often-overlooked symptom that affects up to 80 % of individuals living with PD.
View Article and Find Full Text PDFAdv Sci (Weinh)
January 2025
Tianjin Key Laboratory of Biomedical Materials and Key Laboratory of Biomaterials and Nanotechnology for Cancer Immunotherapy, Institute of Biomedical Engineering, Chinese Academy of Medical Sciences and Peking Union Medical College, Tianjin, 300192, China.
The development of efficient therapeutic strategies to promote ferroptotic cell death offers significant potential for hepatocellular carcinoma (HCC) treatment. Herein, this study presents an HCC-targeted nanoplatform that integrates bimetallic FeMoO nanoparticles with CO-releasing molecules, and further camouflaged with SP94 peptide-modified macrophage membrane for enhanced ferroptosis-driven multi-modal therapy of HCC. Leveraging the multi-enzyme activities of the multivalent metallic elements, the nanoplatform not only decomposes HO to generate oxygen and alleviate tumor hypoxia but also depletes glutathione to inactivate glutathione peroxides 4, which amplify sonodynamic therapy and ferroptotic tumor death under ultrasound (US) irradiation.
View Article and Find Full Text PDFNat Commun
January 2025
Department of Cell Biology, School of Basic Medical Sciences, Cheeloo College of Medicine, Shandong University, Jinan, 250012, China.
Ferroptosis is a newly identified programmed cell death induced by iron-driven lipid peroxidation and implicated as a potential approach for tumor treatment. However, emerging evidence indicates that hepatocellular carcinoma (HCC) cells are generally resistant to ferroptosis and the underlying molecular mechanism is poorly understood. Here, our study confirms that S100 calcium binding protein P (S100P), which is significantly up-regulated in ferroptosis-resistant HCC cells, efficiently inhibits ferroptosis.
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