TY - JOUR
T1 - Electron transport chain dysfunction by H2O2 is linked to increased reactive oxygen species production and iron mobilization by lipoperoxidation
T2 - Studies using Saccharomyces cerevisiae mitochondria
AU - Cortés-Rojo, Christian
AU - Estrada-Villagómez, Mirella
AU - Calderón-Cortés, Elizabeth
AU - Clemente-Guerrero, Mónica
AU - Mejía-Zepeda, Ricardo
AU - Boldogh, Istvan
AU - Saavedra-Molina, Alfredo
N1 - Funding Information:
Acknowledgements The authors appreciate the financial support of grants from CIC-UMSNH 2.16 (ASM), CONACYT (144250 to ASM during his sabbatical), CONACYT 130638 (CCR), PROMEP PTC-266 (CCR), NIEHS RO1 ES18948 (IB), NIAID AI062885-01 (IB), NIA AG 021830 (IB).
PY - 2011/4
Y1 - 2011/4
N2 - The mitochondrial electron transport chain (ETC) contains thiol groups (-SH) which are reversibly oxidized to modulate ETC function during H 2O2 overproduction. Since deleterious effects of H 2O2 are not limited to -SH oxidation, due to the formation of other H2O2-derived species, some processes like lipoperoxidation could enhance the effects of H2O2 over ETC enzymes, disrupt their modulation by -SH oxidation and increase superoxide production. To verify this hypothesis, we tested the effects of H 2O2 on ETC activities, superoxide production and iron mobilization in mitochondria from lipoperoxidation-resistant native yeast and lipoperoxidation-sensitized yeast. Only complex III activity from lipoperoxidation-sensitive mitochondria exhibited a higher susceptibility to H2O2 and increased superoxide production. The recovery of ETC activity by the thiol reductanct β-mercaptoethanol (BME) was also altered at complex III, and a role was attributed to lipoperoxidation, the latter being also responsible for iron release. A hypothetical model linking lipoperoxidation, increased complex III damage, superoxide production and iron release is given.
AB - The mitochondrial electron transport chain (ETC) contains thiol groups (-SH) which are reversibly oxidized to modulate ETC function during H 2O2 overproduction. Since deleterious effects of H 2O2 are not limited to -SH oxidation, due to the formation of other H2O2-derived species, some processes like lipoperoxidation could enhance the effects of H2O2 over ETC enzymes, disrupt their modulation by -SH oxidation and increase superoxide production. To verify this hypothesis, we tested the effects of H 2O2 on ETC activities, superoxide production and iron mobilization in mitochondria from lipoperoxidation-resistant native yeast and lipoperoxidation-sensitized yeast. Only complex III activity from lipoperoxidation-sensitive mitochondria exhibited a higher susceptibility to H2O2 and increased superoxide production. The recovery of ETC activity by the thiol reductanct β-mercaptoethanol (BME) was also altered at complex III, and a role was attributed to lipoperoxidation, the latter being also responsible for iron release. A hypothetical model linking lipoperoxidation, increased complex III damage, superoxide production and iron release is given.
KW - Linolenic acid
KW - Lipid peroxidation
KW - Oxidative stress
KW - Respiratory chain
KW - Thiol oxidation
KW - Yeast
KW - β-mercaptoethanol
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U2 - 10.1007/s10863-011-9339-6
DO - 10.1007/s10863-011-9339-6
M3 - Article
C2 - 21350953
AN - SCOPUS:79958283725
SN - 0145-479X
VL - 43
SP - 135
EP - 147
JO - Journal of Bioenergetics and Biomembranes
JF - Journal of Bioenergetics and Biomembranes
IS - 2
ER -