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* Departamento de Fisiología,
Departamento de Patología, and
Departamento de Bioquímica y Biología Molecular, Universidad de Valencia, 46010 Valencia, Spain
2Correspondence: Departamento de Fisiología, Facultad de Medicina, Avenida Blasco Ibañez 17, 46010 Valencia, Spain. E-mail Federico.V.Pallardo{at}uv.es
Free radicals may be involved in apoptosis although this is the subject of some controversy. Furthermore, the source of free radicals in apoptotic cells is not certain. The aim of this study was to elucidate the role of oxidative stress in the induction of apoptosis in serum-deprived fibroblast cultures and in weaned lactating mammary glands as in vitro and in vivo experimental models, respectively. Oxidative damage to mtDNA is higher in apoptotic cells than in controls. Oxidized glutathione (GSSG) levels in mitochondria from lactating mammary gland are also higher in apoptosis. There is a direct relationship between mtDNA damage and the GSSG/reduced glutathione (GSH) ratio. Furthermore, whole cell GSH is decreased and GSSG is increased in both models of apoptosis. Glutathione oxidation precedes nuclear DNA fragmentation. These signs of oxidative stress are caused, at least in part, by an increase in peroxide production by mitochondria from apoptotic cells. We report a direct relationship between glutathione oxidation and mtDNA damage in apoptosis. Our results support the role of mitochondrial oxidative stress in the induction of apoptosis—Esteve, J. M., Mompo, J., Garcia de la Asuncion, J., Sastre, J., Asensi, M., Boix, J., Viña, J. R., Viña, J., Pallardó, F. V. Oxidative damage to mitochondrial DNA and glutathione oxidation in apoptosis: studies in vivo and in vitro.
Key Words: oxidative stress • mtDNA • mammary gland • glutathione
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