Melatonin, mitochondrial homeostasis and mitochondrial-related diseases.

Abstract

This review examines the role of mitochondria in cellular energy metabolism, heat production via uncoupling mechanisms, and programmed cell death, while also addressing the evolutionary 'hydrogen hypothesis' that posits a symbiotic origin for eukaryotic energy systems. Mitochondria harbor a conserved mammalian genome whose transcription appears responsive to membrane redox potential. Dysfunction in both nuclear and mitochondrial DNA has been implicated in neurodegenerative and neuromuscular conditions. Melatonin, recognized as a potent antioxidant, has accumulated experimental support for protective effects against oxidative stress-induced macromolecular damage, particularly in contexts where mitochondrial integrity is compromised. The review consolidates current mechanistic understanding of melatonin's interactions with mitochondrial pathways.

Mechanism

Melatonin acts as a potent antioxidant that suppresses ROS-induced macromolecular damage and may modulate mitochondrial gene expression through redox-sensitive transcriptional regulation at the mitochondrial membrane, thereby preserving mitochondrial homeostasis.