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Sci Rep. 2018 Oct 18;8(1):15422. doi: 10.1038/s41598-018-33582-w.

Mitochondrial chaotic dynamics: Redox-energetic behavior at the edge of stability.

Author information

1
Instituto de Investigaciones Biológicas y Tecnológicas (IIByT-CONICET), and Instituto de Ciencia y Tecnología de los Alimentos, Cátedra de Química Biológica, Facultad de Ciencias Exactas, Físicas y Naturales, Universidad Nacional de Córdoba, Velez Sarsfield 1611, Córdoba, X5000HUA, Cordoba, Argentina.
2
Laboratory of Cardiovascular Science, National Institute on Aging, NIH. 251 Bayview Boulevard, Baltimore, 21224, MD, USA.
3
School of Biosciences, Cardiff University, Main Building, Museum Avenue, Cardiff, CF10 3AT, Wales, UK.
4
Laboratory of Cardiovascular Science, National Institute on Aging, NIH. 251 Bayview Boulevard, Baltimore, 21224, MD, USA. miguel.aon@nih.gov.

Abstract

Mitochondria serve multiple key cellular functions, including energy generation, redox balance, and regulation of apoptotic cell death, thus making a major impact on healthy and diseased states. Increasingly recognized is that biological network stability/instability can play critical roles in determining health and disease. We report for the first-time mitochondrial chaotic dynamics, characterizing the conditions leading from stability to chaos in this organelle. Using an experimentally validated computational model of mitochondrial function, we show that complex oscillatory dynamics in key metabolic variables, arising at the "edge" between fully functional and pathological behavior, sets the stage for chaos. Under these conditions, a mild, regular sinusoidal redox forcing perturbation triggers chaotic dynamics with main signature traits such as sensitivity to initial conditions, positive Lyapunov exponents, and strange attractors. At the "edge" mitochondrial chaos is exquisitely sensitive to the antioxidant capacity of matrix Mn superoxide dismutase as well as to the amplitude and frequency of the redox perturbation. These results have potential implications both for mitochondrial signaling determining health maintenance, and pathological transformation, including abnormal cardiac rhythms.

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