2009
DOI: 10.1016/j.bbr.2009.07.009
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Social isolation in rats inhibits oxidative metabolism, decreases the content of mitochondrial K-Ras and activates mitochondrial hexokinase

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Cited by 31 publications
(28 citation statements)
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“…The studied enzymes included aconitase, an enzyme from the citrate cycle. As previous studies suggest [21,24], the active center of aconitase is represented by an iron-sulfurous cluster, which is the reason why it shows high sensitivity toward active forms of oxygen. It can be possibly used as a specific marker, sensitive to the oxidative stress.…”
Section: Activity Of Energy Metabolism Enzymes Under Stressmentioning
confidence: 99%
See 1 more Smart Citation
“…The studied enzymes included aconitase, an enzyme from the citrate cycle. As previous studies suggest [21,24], the active center of aconitase is represented by an iron-sulfurous cluster, which is the reason why it shows high sensitivity toward active forms of oxygen. It can be possibly used as a specific marker, sensitive to the oxidative stress.…”
Section: Activity Of Energy Metabolism Enzymes Under Stressmentioning
confidence: 99%
“…) [21]. Activity of creatine kinase was determined by NADH formation following absorbance at 340 nm at 258C.…”
mentioning
confidence: 99%
“…In the meanwhile, these mice showed behavioral changes relevant to some symptoms seen in schizophrenia 97,98 and (5) Ketamine was shown to induce mitochondrial dysfunction, while produced behavioral changes 99 . Moreover, social isolation rearing inhibited oxidative metabolism and induced oxidative stress in rats 100,101 , while it produced several behavioral outcomes similar to those observed in humans with early life stress [100][101][102] . Taken together, these previous studies suggest a connection between mitochondrial dysfunction and neuroinflammation in schizophrenia.…”
Section: Neuroinflammation and Apoptosismentioning
confidence: 52%
“…Mitochondrion is one of the main targets of Ca-dependent Ras-trafficking; however, the functions of K-Ras in mitochondria are not fully understood (Bivona et al 2006;Philips 2006). Our previous observation suggests that the content of mitochondrial K-Ras in hippocampus is changed in various stress conditions (Zhuravliova et al 2009) and delocalization of K-Ras is accompanied by the inhibition of mitochondrial oxidative metabolism. Everything together suggests that the translocation of K-Ras in synaptic mitochondria is a specific response to the energy metabolism impairment in the synaptic endings.…”
Section: Discussionmentioning
confidence: 95%