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Computational modeling demonstrates that nanoparticle membrane laceration drives mitochondrial collapse in cells, indicating physical pollutants can trigger cancer-like metabolic states.
This study presents a non-equilibrium thermodynamic model, formulated via non-linear differential equations, to simulate the phase transition of a differentiated multicellular cell into an atavistic Warburg phenotype following nanoparticle exposure. Inspired by Prigogine’s Brusselator framework, the model demonstrates that physical membrane laceration by tire-wear nano-aggregates acts as a critical bifurcation parameter. The resulting calcium influx collapses mitochondrial respiration, driving the system away from its stable homeostatic steady state and forcing it to settle into a stable limit cycle sustained by autonomous cytoplasmic ATP/NADH oscillations.
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Peter Mikuláš (2026) studied this question.
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