TY - JOUR
T1 - Mitochondrial response to oxidative and nitrosative stress in early stages of diabetes
AU - Noriega-Cisneros, Ruth
AU - Cortés-Rojo, Christian
AU - Manzo-Avalos, Salvador
AU - Clemente-Guerrero, Mónica
AU - Calderón-Cortés, Elizabeth
AU - Salgado-Garciglia, Rafael
AU - Montoya-Pérez, Rocío
AU - Boldogh, Istvan
AU - Saavedra-Molina, Alfredo
N1 - Funding Information:
The authors appreciate the financial support of grants from the UMSNH-CIC ( 2.16 to ASM), CONACYT ( 144250 to ASM during his sabbatical; and 169093 ), CONACYT ( 130638 to CCR), PROMEP ( PTC-266 to CCR) and US NIAID ( AI062885 to IB). We also appreciate the kind gift of polyclonal antibody specific for mitochondrial aconitase from Dr. L.I. Sweda, Oklahoma Medical Research Foundation, OK, USA.
PY - 2013/11
Y1 - 2013/11
N2 - Diabetes mellitus (DM) is associated with increased production of reactive oxygen and nitrogen species; consequently, an increase in lipid peroxidation and a decrease in antioxidants resulting in mitochondrial dysfunction. Using a rat model of DM induced by streptozotocin, we show the opposite: an increase in NO levels, S-nitrosylation, aconitase activity, and total glutathione and a decrease in lipid peroxidation at early stages of diabetes. These data imply that the decrease in lipid peroxidation is a vital early response to hyperglycemia to prevent escalation of ROS generation in mitochondria. These results also suggest a need for novel therapeutic targets to prevent the neurological consequences of diabetes.
AB - Diabetes mellitus (DM) is associated with increased production of reactive oxygen and nitrogen species; consequently, an increase in lipid peroxidation and a decrease in antioxidants resulting in mitochondrial dysfunction. Using a rat model of DM induced by streptozotocin, we show the opposite: an increase in NO levels, S-nitrosylation, aconitase activity, and total glutathione and a decrease in lipid peroxidation at early stages of diabetes. These data imply that the decrease in lipid peroxidation is a vital early response to hyperglycemia to prevent escalation of ROS generation in mitochondria. These results also suggest a need for novel therapeutic targets to prevent the neurological consequences of diabetes.
KW - Antioxidant
KW - Brain mitochondria
KW - Diabetes
KW - Glutathione
KW - Nitrosative stress
KW - Oxidative stress
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U2 - 10.1016/j.mito.2013.05.012
DO - 10.1016/j.mito.2013.05.012
M3 - Article
C2 - 23751425
AN - SCOPUS:84887025517
SN - 1567-7249
VL - 13
SP - 835
EP - 840
JO - Mitochondrion
JF - Mitochondrion
IS - 6
ER -