Heavy Metal Toxicity and Mitochondrial Dysfunction

Ivan Mutebi

Department of Pharmacognosy Kampala International University Uganda

Email: ivan.mutebi@studwc.kiu.ac.ug

                                                                                 ABSTRACT
Heavy metal toxicity remains a critical public health concern due to the widespread presence of metals such as lead, mercury, cadmium, and arsenic in the environment. These metals, even at low concentrations, can exert detrimental effects on biological systems, primarily through the disruption of cellular bioenergetics and redox balance. A growing body of evidence highlights the central role of mitochondrial dysfunction in the pathogenesis of heavy metal toxicity. Mitochondria are essential organelles responsible for energy production, regulation of apoptosis, calcium homeostasis, and reactive oxygen species (ROS) signaling. Exposure to heavy metals can impair mitochondrial function by inhibiting respiratory chain complexes, inducing oxidative stress, disrupting mitochondrial dynamics, and triggering cell death pathways. This review examines the mechanisms through which heavy metals induce mitochondrial dysfunction, explores experimental and clinical findings linking specific metals to mitochondrial damage, and discusses the implications of these disruptions for human health. We also outline emerging strategies for mitigating heavy metal–induced mitochondrial injury, including chelation therapy, antioxidant supplementation, and lifestyle interventions. By integrating current research, this article aims to provide a comprehensive understanding of how heavy metal toxicity intersects with mitochondrial biology and contributes to disease.

Keywords: Heavy metals, Mitochondrial dysfunction, Oxidative stress, Bioenergetics, Toxicology.

CITE AS: Ivan Mutebi. (2026). Heavy Metal Toxicity and Mitochondrial Dysfunction. IDOSR JOURNAL OF SCIENCE AND TECHNOLOGY 12(2):9-14, 2026.
https://doi.org/10.59298/IDOSR/JST/26/122.914