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Carnosine is a naturally occurring endogenous dipeptide composed of beta-alanine and L-histidine, found at high concentrations in human skeletal muscle, heart, and brain tissues [1, 7]. It fulfills diverse biological roles, primarily serving as an intramuscular pH buffer that maintains acid-base homeostasis during intense physical activity [1, 6]. Beyond its buffering capacity, carnosine acts as a multimodal protective agent through its antioxidant, anti-glycation, and metal-chelating properties, which allow it to scavenge reactive oxygen species and prevent the formation of advanced glycation end-products [4, 10, 12]. Due to its neuroprotective and metabolic effects, carnosine is investigated for its potential in treating neurodegenerative disorders like Alzheimer’s disease and complications arising from type 2 diabetes, such as nephropathy [5, 11]. In clinical applications, it is often administered as a dietary supplement or in specialized forms like polaprezinc (zinc-L-carnosine) for gastric protection [8, 13]. Therapeutic strategies aimed at carnosine often focus on enhancing its bioavailability by inhibiting carnosinase 1 (CNDP1), the primary enzyme responsible for its rapid degradation in human serum [8, 12].
As a therapeutic agent, carnosine acts as a pH buffer in muscles and an antioxidant/anti-glycation agent by scavenging reactive carbonyls and oxygen species [1, 2, 4]. It also chelates metal ions like zinc and copper to modulate neurotransmission and enzyme activity [8, 13]. Pharmacological interventions aim to increase carnosine bioavailability through the inhibition of carnosinase enzymes (CNDP1 and CNDP2) or by delivering carnosine as stable complexes or in nanovesicles to bypass enzymatic degradation [8, 12].
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