Cancer, Deuterium, and Autophagy: A Complex Story Unraveled

Stephanie Seneff^1,*, Anthony M. Kyriakopoulos^2,3
1 Computer Science and Artificial Intelligence Laboratory, Massachusetts Institute of Technology, Cambridge, MA, USA
2 Laboratory of Molecular Biology and Immunology, Department of Pharmacy, University of Patras, Rio-Patras, Greece
3 Department of Research and Development, Nasco A.D. Biotechnology Laboratory, Piraeus, Greece
* Corresponding Author: Stephanie Seneff. Email: email
(This article belongs to the Special Issue: Autophagy and Oxidative Stress in Cancer: Molecular Crossroads and Cell Fate Decisions)

BIOCELL https://doi.org/10.32604/biocell.2026.084346

Received 21 April 2026; Accepted 26 June 2026; Published online 20 July 2026

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Abstract

It is increasingly becoming recognized that cancer is primarily a metabolic disease, as manifested by the Warburg effect. Cancer cells exploit their mitochondria to convert the intermediates in the citric acid cycle into resources to support rampant proliferation. Our team has published research claiming that systemic deuterium overload in mitochondria is a risk factor for cancer. Deuterium (heavy hydrogen) is toxic to the F₁F₀-ATP synthase nanomotors in the mitochondria that produce ATP, the energy currency of the cell. Over time, cancer cells become resistant to chemotherapy, and, paradoxically, the resident stromal cells and immune cells assist them in this endeavor. It has been shown that deuterium-enriched water upregulates many cancer-linked proteins in cultured cells, whereas deuterium-depleted water induces oxidative stress in cancer cells and suppresses critical proto-oncogenes, namely, Kirsten rat sarcoma (KRAS) and c-Myc. Treatment of cancer patients with deuterium-depleted water prolongs their lifespan. Our focus here is on the complex role of autophagy and lysosomal dysfunction in the progression of cancer, and the mechanisms by which cells within the tumor microenvironment communicate and share resources through the massive release of exosomes. We finally examine the role of deuterium content in cancer cells during these deregulations.