Evaluation of oxidative stress in d-serine induced nephrotoxicity

Orozco-Ibarra, Marisol; Medina-Campos, Omar Noel; Sánchez-González, Dolores Javier; Martínez-Martínez, Claudia María; Floriano-Sánchez, Esaú; Santamarı́a, Abel; Ramírez, V Mercy; Bobadilla, Norma A.; Pedraza‐Chaverrí, José

doi:10.1016/j.tox.2006.10.008

Cited by 47 publications

(34 citation statements)

References 38 publications

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“…Among the various oxidative modifications of amino acids in proteins, protein carbonyl formation may be an early marker for protein oxidation [44]. Recent research supports the point that protein carbonyl derivatives are formed during nephrotoxicity as a consequence of oxidant stress [45,46].…”

Section: Discussionmentioning

confidence: 95%

Protective effect of lipoic acid on oxidative and peroxidative damage in cyclosporine A-induced renal toxicity

Amudha

Josephine

Sudhahar

et al. 2007

International Immunopharmacology

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Section: Discussionmentioning

confidence: 95%

Protective effect of lipoic acid on oxidative and peroxidative damage in cyclosporine A-induced renal toxicity

Amudha

Josephine

Sudhahar

et al. 2007

International Immunopharmacology

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“…2b). This may be explained because DAO/D-serine induces GSH depletion (Krug et al 2007;Orozco-Ibarra et al 2007). Pyruvate becomes toxic to cells when glutathione is depleted (Marí et al 2002).…”

Section: Discussionmentioning

confidence: 99%

3-Bromopyruvate antagonizes effects of lactate and pyruvate, synergizes with citrate and exerts novel anti-glioma effects

Sayed

El-Magd

Shishido

et al. 2012

J Bioenerg Biomembr

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Oxidative stress-energy depletion therapy using oxidative stress induced by D-amino acid oxidase (DAO) and energy depletion induced by 3-bromopyruvate (3BP) was reported recently (El Sayed et al., Cancer Gene Ther., 19, 1-18, 2012). Even in the presence of oxygen, cancer cells oxidize glucose preferentially to produce lactate (Warburg effect) which seems vital for cancer microenvironment and progression. 3BP is a closely related structure to lactate and pyruvate and may antagonize their effects as a novel mechanism of its action. Pyruvate exerted a potent H(2)O(2) scavenging effect to exogenous H(2)O(2), while lactate had no scavenging effect. 3BP induced H(2)O(2) production. Pyruvate protected against H(2)O(2)-induced C6 glioma cell death, 3BP-induced C6 glioma cell death but not against DAO/D-serine-induced cell death, while lactate had no protecting effect. Lactate and pyruvate protected against 3BP-induced C6 glioma cell death and energy depletion which were overcome with higher doses of 3BP. Lactate and pyruvate enhanced migratory power of C6 glioma which was blocked by 3BP. Pyruvate and lactate did not protect against C6 glioma cell death induced by other glycolytic inhibitors e.g. citrate (inhibitor of phosphofructokinase) and sodium fluoride (inhibitor of enolase). Serial doses of 3BP were synergistic with citrate in decreasing viability of C6 glioma cells and spheroids. Glycolysis subjected to double inhibition using 3BP with citrate depleted ATP, clonogenic power and migratory power of C6 glioma cells. 3BP induced a caspase-dependent cell death in C6 glioma. 3BP was powerful in decreasing viability of human glioblastoma multiforme cells (U373MG) and C6 glioma in a dose- and time-dependent manner.

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“…In contrast to Akt and mTOR signaling, MAPK and ERK (Table 1) signaling were not altered in the hippocampus of SR −/− mice. We also examined the kidneys of these mice because a single dose of Dserine (400 mg/kg) leads to transient nephrotoxicity in rats due to high levels of D-amino acid oxidase in the proximal tubules (48). We found that our chronic D-serine dosing regimen had no deleterious effects on the kidneys (Fig.…”

Section: +mentioning

confidence: 97%

Multiple risk pathways for schizophrenia converge in serine racemase knockout mice, a mouse model of NMDA receptor hypofunction

Balu

Puhl

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

199

201

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Schizophrenia is characterized by reduced hippocampal volume, decreased dendritic spine density, altered neuroplasticity signaling pathways, and cognitive deficits associated with impaired hippocampal function. We sought to determine whether this diverse pathology could be linked to NMDA receptor (NMDAR) hypofunction, and thus used the serine racemase-null mutant mouse (SR −/− ), which has less than 10% of normal brain D-serine, an NMDAR coagonist. We found that D-serine was necessary for the maintenance of long-term potentiation in the adult hippocampal dentate gyrus and for full NMDAR activity on granule cells. SR −/− mice had reduced dendritic spines and hippocampal volume. These morphological changes were paralleled by diminished BDNF/Akt/mammalian target of rapamycin (mTOR) signaling and impaired performance on a traceconditioning memory task. Chronic D-serine treatment normalized the electrophysiological, neurochemical, and cognitive deficits in SR −/− mice. These results demonstrate that NMDAR hypofunction can reproduce the numerous hippocampal deficits associated with schizophrenia, which can be reversed by chronic peripheral D-serine treatment.miR-132 | MeCP2 | glycogen synthase 3 kinase | CREB S chizophrenia is a severe psychiatric disorder that affects 1% of the population worldwide (1). There are widespread morphological, neurochemical, and functional changes in the brain in schizophrenia that have been linked to its symptomatic features (2). For example, the hippocampus of patients with schizophrenia exhibits reduced dendritic spine density (3), atrophy (4), and impaired activation while performing cognitive tasks (5). The neuroplasticity deficits observed in schizophrenia could be caused by a constellation of factors.Impaired neurotrophic signaling could be one mechanism underlying these abnormalities. BDNF regulates a complex array of processes, including neurite outgrowth and spine density, by signaling through tropomyosin receptor kinase B (TrkB), its highaffinity receptor (6). In postmortem studies, BDNF mRNA and protein (7-9) levels, as well as TrkB mRNA (7, 10, 11) and protein (12), are reduced in subjects with schizophrenia. V-akt murine thymoma viral oncogene (Akt) is a kinase downstream of TrkB. Not only is the Akt1 isoform a putative schizophrenia risk gene (13), its expression (14, 15) and the amount of phosphorylated Akt (p-Akt) (16) in the dentate gyrus (DG) are reduced in schizophrenia.Aberrant microRNA (miR) processing might also be contributing to the pathophysiology of schizophrenia (17). These noncoding RNAs regulate neural plasticity by controlling the translation of target mRNA transcripts. Expression of the neuron-enriched miR-132 is reduced in schizophrenia (18); it regulates basal and activityinduced neurite outgrowth (19), and is up-regulated in vivo in response to external stimuli (20, 21). Importantly, both BDNF (22) and miR-132 (17) expression are increased by NMDAR receptor (NMDAR) activation.Pharmacologic and biochemical evidence has converged to support NMDAR hypofunct...

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Evaluation of oxidative stress in d-serine induced nephrotoxicity

Cited by 47 publications

References 38 publications

Protective effect of lipoic acid on oxidative and peroxidative damage in cyclosporine A-induced renal toxicity

Protective effect of lipoic acid on oxidative and peroxidative damage in cyclosporine A-induced renal toxicity

3-Bromopyruvate antagonizes effects of lactate and pyruvate, synergizes with citrate and exerts novel anti-glioma effects

Multiple risk pathways for schizophrenia converge in serine racemase knockout mice, a mouse model of NMDA receptor hypofunction

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