Abstract
Mitochondria play a fundamental role in the energy metabolism of eukaryotic cells. Numerous studies indicate lead (Pb) as a widely occurring environmental factor capable of disrupting oxidative metabolism by modulating the mitochondrial processes. The multitude of known molecular targets of Pb and its strong affinity for biochemical pathways involving divalent metals suggest that it may pose a health threat at any given dose. Changes in the bioenergetics of cells exposed to Pb have been repeatedly demonstrated in research, primarily showing a reduced ability to synthesize ATP. In addition, lead interferes with mitochondrial-mediated processes essential for maintaining homeostasis, such as apoptosis, mitophagy, mitochondrial dynamics, and the inflammatory response. This article describes selected aspects of mitochondrial metabolism in relation to potential mechanisms of energy metabolism disorders induced by Pb.
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