メラトニンとミトコンドリア恒常性：ミトコンドリア関連疾患における役割のレビュー
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.
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.
The delivery route is not clearly identifiable from this paper. For hydrogen intake, inhalation is the most efficient route; inhalation, however, carries explosion risk (empirical LFL of 10%; high-concentration devices are not recommended).
See also:
https://h2-papers.org/en/papers/11899097