Helios Pareja-Galeano, Alejandro Santos-Lozano, María Morán, Fabian Sanchis-Gomar, Rafael Alis, Alfredo Santalla, Alejandro F. San Juan, Jorge Díez-Bermejo, Miguel A. Martín, Joaquín Arenas and Alejandro Lucia Pages 2657 - 2663 ( 7 )
The intent of this article is to summarize current body of knowledge on the potential implication of the xanthine oxidase pathway (XO) on skeletal muscle damage. The possible involvement of the XO pathway in muscle damage is exemplified by the role of XO inhibitors (e.g., allopurinol) in attenuating muscle damage. Reliance on this pathway (as well as on the purine nucleotide cycle) could be exacerbated in conditions of low muscle glycogen availability. Thus, we also summarize current hypotheses on the etiology of both baseline and exertional muscle damage in McArdle disease, a condition caused by inherited deficiency of myophosphorylase. Because myophosphorylase catalyzes the first step of muscle glycogen breakdown, patients are unable to obtain energy from their muscle glycogen stores. Finally, we provide preliminary data from our laboratory on the potential implication of the XO pathway in the muscle damage that is commonly experienced by these patients.
McArdle disease, xanthine oxidase, muscle damage, rhabdomyolysis, oxidative stress.
, , , Research Institute of Hospital 12 de Octubre (i+12), 6th Floor, Laboratories Sector, CAA Building, Avda. de Córdoba s/n, 28041 Madrid, Spain.