2010
DOI: 10.1016/j.neuropharm.2009.12.009
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Decreased glutathione levels and altered antioxidant defense in an animal model of schizophrenia: Long-term effects of perinatal phencyclidine administration

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Cited by 71 publications
(41 citation statements)
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“…Previous studies have shown a decrease in the GSH level in CSF in drug-naive patients and in animal models of schizophrenia, supporting the hypothesis of an impaired antioxidant defence system in the pathophysiology of the disorder (Do et al, 2000;Radonjić et al, 2010). In contrast to those studies, we did not find any differences in GSH levels in plasma or CSF between patients and controls.…”
Section: Discussionsupporting
confidence: 62%
“…Previous studies have shown a decrease in the GSH level in CSF in drug-naive patients and in animal models of schizophrenia, supporting the hypothesis of an impaired antioxidant defence system in the pathophysiology of the disorder (Do et al, 2000;Radonjić et al, 2010). In contrast to those studies, we did not find any differences in GSH levels in plasma or CSF between patients and controls.…”
Section: Discussionsupporting
confidence: 62%
“…This indicates different degrees of oxidative stress in different brain areas in schizophrenics. Radonjic, et al [8] confirmed this finding in animal studies in which phencyclidine-fed perinatal Wister rats were used to produce schizophrenic animal models. It was found that lipid peroxidation levels in the hippocampus and thalamus areas were significantly increased.…”
Section: Elevated Indicator Level Of Oxidative Stress In Schizophreniamentioning
confidence: 78%
“…In animal models of schizophrenia, perinatal phencyclidine (an NMDA receptor antagonist) administration increased the level of lipid peroxides in rats [124], while ketamine (an NMDA antagonist) injections to mice increased lipid [125,126] and protein [126] peroxidation and raised superoxide levels [127]. In genetic models, there were either increased levels of oxidized lipids in G72/G30 transgenic schizophrenic mice [128] or elevated cortical ROS production in g-aminobutyric acid-ergic interneuron-specific NMDAR hypofunction mice (Ppp1r2-Cre/ fGluN1 knockout [KO] mice) [129] (Table 1).…”
Section: Animal Studiesmentioning
confidence: 99%
“…Perinatal phencyclidine or ketamine administration to rodents evoked depletion of the reduced GSH and several changes in enzymes activities [124,126] (see Table 1). In genetic models, there are several lines of evidence that oxidative stress plays a role in the pathogenesis of schizophrenia.…”
Section: Animal Studiesmentioning
confidence: 99%