SLIDE 1: “Title & Motivation”
• Title: “Quantum Biological Electron Tunneling (QBET) in Living Systems”
• Motivation: Investigate how electron tunneling at the sub-nanometer scale manifests in biomolecule–nanoparticle systems.
• Why It Matters: QBET reveals real-time redox changes of cytochrome c (Cyt c), which are crucial for understanding cell-death pathways and broader biochemical processes.
[1] [2]
SLIDE 2: “Background & Theory”
• What is Quantum Tunneling?
– Electron wavefunctions can penetrate barriers “forbidden” classically, with probability decaying exponentially as barrier width increases.
• Biological Context: Cytochrome c’s oxidized (Ox.) and reduced (Red.) states are important markers in apoptosis and other metabolic processes.
• Tunneling in Biological Systems: The sub-nanometer linkers between nanoparticles and biomolecules set the stage for measuring QBET directly.
[3] [4]
SLIDE 3: “Project Setup: QBET Method”
• A/B/C Tunnel Junction:
– A = Gold Nanoparticle (GNP), B = Linker Molecule, C = Cytochrome c
• Quantized Dips in Scattering Spectra:
– ~530 nm (Ox. Cyt c), ~520 & ~550 nm (Red. Cyt c)
– Indicates electron tunneling from GNP into distinct electronic states of Cyt c.
• Plasmonic Enhancement: Local field around GNP can speed up redox transitions.
[5] [6]
SLIDE 4: “Key Observations & Data”
• Spectral Shifts in Real Time:
– Shows transition from Ox. to Red. form of Cyt c under reductants like dithionite.
• Intracellular Measurements: Cells undergoing apoptosis vs. necrosis exhibit unique, time-dependent spectral signatures.
• Reaction Rate Comparison: QBET often proceeds faster than in bulk solution, indicating possible catalytic effects.
[7] [8]
SLIDE 5: “Conclusions”
• Non-Invasive Real-Time Probe: QBET spectroscopy gives a wireless way to monitor electron transfer inside living cells.
• Apoptosis vs. Necrosis: Differences in Cyt c redox transitions enable this method to distinguish cell-death pathways.
• Broader Significance: Could be generalized to other redox-active biomolecules, offering insights into metabolic oscillations and disease states.
[9]
SLIDE 6: “Limitations”
• Exponential Decay with Barrier Width: Minor increases in linker thickness drastically reduce tunneling probability.
• Heterogeneity in Live Cells: Intracellular conditions (e.g., pH, competing redox events) can complicate data interpretation.
• Sample Preparation: Achieving uniform sub-nanometer control over barrier thickness is difficult.
• Theoretical Complexity: Multi-electron hopping and altered barrier heights may cause deviations from simple single-electron models.
[10]
SLIDE 7: “Next Steps”
• Expand to Other Biomolecules: QBET could be applied to diverse redox enzymes—NADH, FAD, etc.
• Enhanced Instrumentation: Develop advanced nanoscopy and single-particle tracking to improve resolution and signal.
• Diagnostic Applications: Investigate how QBET signals might detect early metabolic dysregulation or cell-death signatures in clinical samples.
• Refining Linker Chemistry: Employ linkers with optimized HOMO-LUMO gaps to boost tunneling efficiency.
[11]
SLIDE 8: “Short Answer Question & Answer”
Short Answer Q:
“How does QBET distinguish between apoptosis and necrosis in cells?”
Answer:
“QBET captures the evolving redox status of Cyt c through dips at ~530 nm (oxidized) and ~520/550 nm (reduced). Apoptosis produces a regulated, stepwise shift in these dips, reflecting a controlled Cyt c release. Necrosis, by contrast, is more abrupt and disorganized. Thus, the distinct dip patterns separate apoptotic from necrotic cell-death pathways.”SLIDE 1: “Title & Motivation”
• Title: “Quantum Biological Electron Tunneling (QBET) in Living Systems”
• Motivation: Investigate how electron tunneling at the sub-nanometer scale manifests in biomolecule–nanoparticle systems.
• Why It Matters: QBET reveals real-time redox changes of cytochrome c (Cyt c), which are crucial for understanding cell-death pathways and broader biochemical processes.
[1] [2]
SLIDE 2: “Background & Theory”
• What is Quantum Tunneling?
– Electron wavefunctions can penetrate barriers “forbidden” classically, with probability decaying exponentially as barrier width increases.
• Biological Context: Cytochrome c’s oxidized (Ox.) and reduced (Red.) states are important markers in apoptosis and other metabolic processes.
• Tunneling in Biological Systems: The sub-nanometer linkers between nanoparticles and biomolecules set the stage for measuring QBET directly.
[3] [4]
SLIDE 3: “Project Setup: QBET Method”
• A/B/C Tunnel Junction:
– A = Gold Nanoparticle (GNP), B = Linker Molecule, C = Cytochrome c
• Quantized Dips in Scattering Spectra:
– ~530 nm (Ox. Cyt c), ~520 & ~550 nm (Red. Cyt c)
– Indicates electron tunneling from GNP into distinct electronic states of Cyt c.
• Plasmonic Enhancement: Local field around GNP can speed up redox transitions.
[5] [6]
SLIDE 4: “Key Observations & Data”
• Spectral Shifts in Real Time:
– Shows transition from Ox. to Red. form of Cyt c under reductants like dithionite.
• Intracellular Measurements: Cells undergoing apoptosis vs. necrosis exhibit unique, time-dependent spectral signatures.
• Reaction Rate Comparison: QBET often proceeds faster than in bulk solution, indicating possible catalytic effects.
[7] [8]
SLIDE 5: “Conclusions”
• Non-Invasive Real-Time Probe: QBET spectroscopy gives a wireless way to monitor electron transfer inside living cells.
• Apoptosis vs. Necrosis: Differences in Cyt c redox transitions enable this method to distinguish cell-death pathways.
• Broader Significance: Could be generalized to other redox-active biomolecules, offering insights into metabolic oscillations and disease states.
[9]
SLIDE 6: “Limitations”
• Exponential Decay with Barrier Width: Minor increases in linker thickness drastically reduce tunneling probability.
• Heterogeneity in Live Cells: Intracellular conditions (e.g., pH, competing redox events) can complicate data interpretation.
• Sample Preparation: Achieving uniform sub-nanometer control over barrier thickness is difficult.
• Theoretical Complexity: Multi-electron hopping and altered barrier heights may cause deviations from simple single-electron models.
[10]
SLIDE 7: “Next Steps”
• Expand to Other Biomolecules: QBET could be applied to diverse redox enzymes—NADH, FAD, etc.
• Enhanced Instrumentation: Develop advanced nanoscopy and single-particle tracking to improve resolution and signal.
• Diagnostic Applications: Investigate how QBET signals might detect early metabolic dysregulation or cell-death signatures in clinical samples.
• Refining Linker Chemistry: Employ linkers with optimized HOMO-LUMO gaps to boost tunneling efficiency.
[11]
SLIDE 8: “Short Answer Question & Answer”
Short Answer Q:
“How does QBET distinguish between apoptosis and necrosis in cells?”
Answer:
“QBET captures the evolving redox status of Cyt c through dips at ~530 nm (oxidized) and ~520/550 nm (reduced). Apoptosis produces a regulated, stepwise shift in these dips, reflecting a controlled Cyt c release. Necrosis, by contrast, is more abrupt and disorganized. Thus, the distinct dip patterns separate apoptotic from necrotic cell-death pathways.”