Synopsis

Source of validity: Scientific
Rating (out of 5): 3

L-glutathione is a tripeptide composed of glutamine, cysteine, and glycine, and it plays a crucial role in cellular redox balance and antioxidant defense. Its relevance to mitochondrial health stems from its function as the most abundant intracellular antioxidant, particularly significant within the mitochondria, where oxidative phosphorylation generates reactive oxygen species (ROS). Excessive ROS can damage mitochondrial proteins, lipids, and DNA, leading to impaired energy production and cellular dysfunction. L-glutathione helps neutralize these ROS, thereby protecting mitochondrial integrity. Scientific studies have demonstrated that depleted glutathione levels are associated with mitochondrial dysfunction in various disease models, including neurodegenerative and metabolic disorders. Experimental supplementation or upregulation of glutathione has been shown to restore mitochondrial function and reduce oxidative damage in animal and cell studies. However, robust clinical trials in humans supporting the direct use of supplemental L-glutathione for mitochondrial health remain limited. The majority of human evidence is indirect, linking low glutathione status with poor mitochondrial function rather than demonstrating clear clinical benefits from supplementation. In summary, there is a well-established scientific rationale for glutathione’s central role in mitochondrial protection and redox balance, supported by preclinical and mechanistic studies. However, the clinical evidence for direct health benefits from exogenous L-glutathione supplementation for mitochondrial support in humans is still emerging and not definitive.

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