ArticleJACS Au2024
Proton Tunneling Allows a Proton-Coupled Electron Transfer Process in the Cancer Cell.
Article in JACS Au, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed.
- Irreversible NADH Cleavage by a Mitochondria-Targeted Metal-Free Photoredox Sensitizer with Activity in Cancer Cells.ACS medicinal chemistry letters · 2026Article
- Quantum medicine: A quantum-mechanical framework for redox biology, disease and precision medicine.Clinical and translational medicine · 2026Review
- Modelling double proton tunneling along low-barrier hydrogen bonds through time-dependent Fourier grid Hamiltonian method.Journal of molecular modeling · 2025Article
- Red-Light-Mediated Generation of Radicals: Applications in Organic Synthesis, Small-Molecule Activation, Polymerization, and Bio-Related Fields.Angewandte Chemie (International ed. in English) · 2025Review
- Nrf1 acts as a highly-conserved determinon for maintaining robust redox homeostasis in the eco-evo-devo process of life histories.Cell stress · 2025Review
Corrections and comments
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Authors and funding
12 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proton-coupled electron transfer (PCET) is a fundamental redox process and has clear advantages in selectively activating challenging C-H bonds in many biological processes. Intrigued by this activation process, we aimed to develop a facile PCET process in cancer cells by modulating proton tunneling. This approach should lead to the design of an alternative photodynamic therapy (PDT) that depletes the mitochondrial electron transport chain (ETC), the key redox regulator in cancer cells under hypoxia. To observe this depletion process in the cancer cell, we monitored the oxidative-stress-induced depolarization of mitochondrial inner membrane potential (MMP) using fluorescence lifetime imaging microscopy (FLIM). Typically, increasing metabolic stress of cancer cells is reflected in a nontrivial change in the fluorophore's fluorescence lifetime. After 30 min of irradiation, we observed a shift in the mean lifetime value and a drastic drop in overall fluorescence signal. In addition, our PCET strategy resulted in drastic reorganization of mitochondrial morphology from tubular to vesicle-like and causing an overall depletion of intact mitochondria in the hypodermis of
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Registered trials
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