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The role of tetrahydroxyquinone solubility on apoptosis induction in human colorectal cells.
Toxicol Mech Methods
January 2025
Cell Biology Laboratory, Centro Universitario de la Ciénega, Universidad de Guadalajara, Ocotlán, Mexico.
Tetrahydroxy-1,4-benzoquinone (THQ) is a highly redox-active substance that generates reactive oxygen species (ROS), which can induce apoptosis in cell culture experiments. The underlying mechanism for ROS production has previously been postulated to be the autoxidation of THQ to rhodizonic acid (RhA). However, our results suggest that the cells detoxify THQ by reducing it to hexahydroxybenzene (HHB), catalyzed by the NADPH-quinone-oxidoreductase (NQO1).
View Article and Find Full Text PDFIn defence of ferroptosis.
Signal Transduct Target Ther
January 2025
The Florey Institute of Neuroscience and Mental Health, Melbourne, VIC, Australia.
Rampant phospholipid peroxidation initiated by iron causes ferroptosis unless this is restrained by cellular defences. Ferroptosis is increasingly implicated in a host of diseases, and unlike other cell death programs the physiological initiation of ferroptosis is conceived to occur not by an endogenous executioner, but by the withdrawal of cellular guardians that otherwise constantly oppose ferroptosis induction. Here, we profile key ferroptotic defence strategies including iron regulation, phospholipid modulation and enzymes and metabolite systems: glutathione reductase (GR), Ferroptosis suppressor protein 1 (FSP1), NAD(P)H Quinone Dehydrogenase 1 (NQO1), Dihydrofolate reductase (DHFR), retinal reductases and retinal dehydrogenases (RDH) and thioredoxin reductases (TR).
View Article and Find Full Text PDFImpact of c-JUN deficiency on thalamus development in mice and human neural models.
Cell Biosci
December 2024
Key Laboratory of Biological Targeting Diagnosis, Therapy and Rehabilitation of Guangdong Higher Education Institutes, The Fifth Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Article Synopsis
- c-Jun is essential for regulating gene expression and plays a significant role in embryonic development, particularly in the nervous system, yet its effects on deep brain structures like the thalamus are not well understood.
- Using c-Jun knockout (KO) models and various cell cultures, researchers investigated its impact on nervous system development, revealing that c-Jun KO mice exhibited underdeveloped thalamus structures and disrupted neuronal connectivity.
- The study concluded that the absence of c-JUN leads to impaired nerve fiber extension and abnormal thalamus patterning, highlighting the importance of c-JUN in embryonic neural development.
Nrf2 induction potency of plant-derived compounds determined using an antioxidant response element luciferase reporter and conventional NAD(P)H-quinone acceptor oxidoreductase 1 activity assay.
BMC Res Notes
December 2024
Department of Vegetable Life Science, Graduate School of Medicine, Hirosaki University, 5 Zaifu-cho, Hirosaki, 036-8562, Aomori, Japan.
Objective: Various plants have been reported to contain compounds that promote the transcriptional activity of Nuclear factor erythroid 2-related factor 2 (Nrf2) to induce a set of xenobiotic detoxifying enzymes, such as NAD(P)H-quinone acceptor oxidoreductase 1 (NQO1), via the antioxidant response element (ARE). While conventional methods for evaluating Nrf2 induction potency include measurement of NQO1 activity, an ARE luciferase reporter assay was recently developed to specifically assess Nrf2 induction potency of compounds of interest. In this study, we compared the abilities of these two assays to evaluate and determine Nrf2 induction potency of plant-derived compounds.
View Article and Find Full Text PDFAltered hypoxia- and redox-related transcriptional signatures in mitochondrial-DNA-depleted PC-3 cells.
Biochem Biophys Res Commun
January 2025
Department of Biological Sciences, Brock University, St. Catharines, ON, L2S 3A1, Canada. Electronic address:
Rho 0 (ρ) cells are widely used as a tool to investigate how the absence of respiring mitochondria affects a variety of physiological and pathological processes. Prominently, ρ cells have been used to study the role of mitochondrial reactive oxygen species (ROS) production and/or mitochondrial respiration in the stabilization of the hypoxia-inducible factor (HIF) in hypoxia. In this study, we cultured ρ and WT PC-3 cells in 5% O (physioxia) and Plasmax medium for 2 weeks prior to transcriptomic and functional analyses.
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