PROIMI   05436
PLANTA PILOTO DE PROCESOS INDUSTRIALES MICROBIOLOGICOS
Unidad Ejecutora - UE
artículos
Título:
Yeast frataxin mutants display decreased superoxide dismutase activity crucial to promote protein oxidative damage
Autor/es:
VERÓNICA IRAZUSTA; ELIA OBIS; ARMANDO MORENO-CERMEÑO; ELISA CABISCOL; JOAQUIM ROS; JORDI TAMARIT
Revista:
FREE RADICAL BIOLOGY AND MEDICINE
Editorial:
ELSEVIER
Referencias:
Año: 2010 vol. 48 p. 411 - 420
ISSN:
0891-5849
Resumen:
Iron overload is involved in several pathological conditions, including Friedreich ataxia, a disease caused by
decreased expression of the mitochondrial protein frataxin. In a previous study, we identified 14 proteins
selectively oxidized in yeast cells lacking Yfh1, the yeast frataxin homolog. Most of these were magnesiumbinding
proteins. Decreased Mn-SOD activity, oxidative damage to CuZn-SOD, and increased levels of
chelatable iron were also observed in this model. This study explores the relationship between low SOD
activity, the presence of chelatable iron, and protein damage. We observed that addition of copper and
manganese to the culture medium restored SOD activity and prevented both oxidative damage and
inactivation of magnesium-binding proteins. This protection was compartment specific: recovery of
mitochondrial enzymes required the addition of manganese, whereas cytosolic enzymes were recovered by
adding copper. Copper treatment also decreased Äyfh1 sensitivity to menadione. Finally, a Äsod1 mutant
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
mitochondrial enzymes required the addition of manganese, whereas cytosolic enzymes were recovered by
adding copper. Copper treatment also decreased Äyfh1 sensitivity to menadione. Finally, a Äsod1 mutant
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
selectively oxidized in yeast cells lacking Yfh1, the yeast frataxin homolog. Most of these were magnesiumbinding
proteins. Decreased Mn-SOD activity, oxidative damage to CuZn-SOD, and increased levels of
chelatable iron were also observed in this model. This study explores the relationship between low SOD
activity, the presence of chelatable iron, and protein damage. We observed that addition of copper and
manganese to the culture medium restored SOD activity and prevented both oxidative damage and
inactivation of magnesium-binding proteins. This protection was compartment specific: recovery of
mitochondrial enzymes required the addition of manganese, whereas cytosolic enzymes were recovered by
adding copper. Copper treatment also decreased Äyfh1 sensitivity to menadione. Finally, a Äsod1 mutant
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
mitochondrial enzymes required the addition of manganese, whereas cytosolic enzymes were recovered by
adding copper. Copper treatment also decreased Äyfh1 sensitivity to menadione. Finally, a Äsod1 mutant
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
fied 14 proteins
selectively oxidized in yeast cells lacking Yfh1, the yeast frataxin homolog. Most of these were magnesiumbinding
proteins. Decreased Mn-SOD activity, oxidative damage to CuZn-SOD, and increased levels of
chelatable iron were also observed in this model. This study explores the relationship between low SOD
activity, the presence of chelatable iron, and protein damage. We observed that addition of copper and
manganese to the culture medium restored SOD activity and prevented both oxidative damage and
inactivation of magnesium-binding proteins. This protection was compartment specific: recovery of
mitochondrial enzymes required the addition of manganese, whereas cytosolic enzymes were recovered by
adding copper. Copper treatment also decreased Äyfh1 sensitivity to menadione. Finally, a Äsod1 mutant
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would
also apply to pathologies involving iron accumulation.
showed high levels of chelatable iron and inactivation of magnesium-binding enzymes. These results suggest
that reduced superoxide dismutase activity contributes to the toxic effects of iron overloading. This would