Effect of quinolinic acid on endogenous antioxidants in rat corpus striatum

Rodrı́guez-Martı́nez, Erika; Camacho, Alberto; Maldonado, Perla D.; Pedraza‐Chaverrí, José; Santamaría, Daniel; Galván‐Arzate, Sonia; Santamarı́a, Abel

doi:10.1016/s0006-8993(99)02474-9

Cited by 111 publications

(71 citation statements)

References 15 publications

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“…concentrations, loss of ATP and cell death (Stone 1993). On the other hand, a number of studies indicated that QA induce significant oxidative damage in brain tissue particularly striatum (Rodríguez-Martínez et al 2000;Cabrera et al 2000). Our results also highlighted the ex vivo increase in lipid peroxidation, nitrite concentration, decreased SOD as well as catalase enzyme activities by QA in rat striatum, suggesting oxidative damage in the striatum.…”

Section: Discussionsupporting

confidence: 70%

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Kalonia

Kumar

et al. 2009

Inflammopharmacol

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Oxidative stress has long been implicated in the neurotoxic effects of glutamate acting through N-methyl-D-aspartate (NMDA) receptors. Therefore, present study has been designed to explore the effect of rofecoxib and caffeic acid on the involvement of oxidative stress, mitochondrial dysfunction and neuronal linked with NMDA receptor-mediated excitotoxicity. Caffeic acid, is a well-known antioxidant flavanoid, implicate anti-inflammatory and immunomodulatory like actions. The present study is an attempt to investigate the antioxidant-like effect of caffeic acid and rofecoxib and their combination against QA-induced oxidative damage, mitochondrial dysfunction and histological alterations. Intrastriatal injection of quinolinic acid (300 nmol) significantly increased oxidative stress (raised lipid peroxidation, nitrite concentration, depleted SOD and catalase), altered mitochondrial complex enzyme activities and histological alteration in the ex vivo striatum. Caffeic acid (5 and 10 mg/kg, p.o.) and rofecoxib (10 and 20 mg/kg, p.o.) treatment for 21 days significantly attenuated oxidative damage and impairment in mitochondrial activities of complex enzymes in the ex vivo striatum. Further, combination of sub effective doses of rofecoxib (10 mg/kg, p.o.) and caffeic acid (5 mg/kg, p.o.) potentiated their protective effect which was significant as compared to their effect per se. The present study suggests the therapeutic effect of caffeic acid and rofecoxib combination against QA-induced ex vivo oxidative damage, mitochondrial and histological alterations in rats.

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Section: Discussionsupporting

confidence: 70%

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Kalonia

Kumar

et al. 2009

Inflammopharmacol

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“…Recent studies focused mainly on the early post-injection effects (Bordelon et al, 1998;Bordelon and Chesselet, 1999;Ceresoli-Borroni et al, 1999;Mena et al, 2000;Rodriguez-Martinez et al, 2000). We chose a protocol (5 days post-injection, 150 nmol QA dose) because this dose has been shown to induce significant neuropathology and behavioral deficits that are amenable to treatment.…”

mentioning

confidence: 99%

Metabolic changes in quinolinic acid‐lesioned rat striatum detected non‐invasively by in vivo ¹H NMR spectroscopy

Tkáč

Keene

Pfeuffer

et al. 2001

J of Neuroscience Research

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Intrastriatal injection of quinolinic acid (QA) provides an animal model of Huntington disease. In vivo 1 H NMR spectroscopy was used to measure the neurochemical profile non-invasively in seven animals 5 days after unilateral injection of 150 nmol of QA. Concentration changes of 16 metabolites were measured from 22 l volume at 9.4 T. The increase of glutamine ((ϩ25 Ϯ 14)%, mean Ϯ SD, n ϭ 7) and decrease of glutamate (Ϫ12 Ϯ 5)%, N-acetylaspartate (Ϫ17 Ϯ 6)%, taurine (Ϫ14 Ϯ 6)% and total creatine (Ϫ9 Ϯ 3%) were discernible in each individual animal (P Ͻ 0.005, paired t-test). Metabolite concentrations in control striata were in excellent agreement with biochemical literature. The change in glutamate plus glutamine was not significant, implying a shift in the glutamate-glutamine interconversion, consistent with a metabolic defect at the level of neuronal-glial metabolic trafficking. The most significant indicator of the lesion, however, were the changes in glutathione ((Ϫ19 Ϯ 9)%, P Ͻ 0.002)), consistent with oxidative stress. From a comparison with biochemical literature we conclude that high-resolution in vivo 1 H NMR spectroscopy accurately reflects the neurochemical changes induced by a relatively modest dose of QA, which permits one to longitudinally follow mitochondrial function, oxidative stress and glial-neuronal metabolic trafficking as well as the effects of treatment in this model of Huntington disease.

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“…However, although MK-801 reduced the malonate-induced lesion volume in the striatum, it did not block the generation of reactive oxygen species (ROS), indicating that NMDA receptor activation occurs but does not result in the generation of ROS in malonate toxicity (6,7). In contrast with this, other studies have shown that NMDA receptors activation could be involved in the observed increased in ROS levels (8,9), thus contributing to oxidative stress due to malonate.…”

Section: Introductionmentioning

confidence: 93%

“…Taking into account that in vivo and in vitro QA can exacerbate considerably the production of ROS and lipid peroxidation (17,21,22) and that lipid peroxidation is initiated by the attack of free radicals against unsaturated membrane lipids, it is reasonable assume that QA toxicity is mediated by ROS formed after NMDA receptors activation (8,9). In addition, QA-induced lipid peroxidation is blocked by MK-801 and a variety of antioxidants (9,(22)(23)(24)(25)(26)(27)(28) giving further support for NMDA receptor activation and ROS overproduction on its toxicity.…”

Section: Introductionmentioning

confidence: 99%

N-methyl-D-aspartate Receptors are Involved in the Quinolinic Acid, but not in the Malonate Pro-oxidative Activity in vitro

2005

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Oxidative stress plays a significant role in the neurotoxicity of a variety of agents that interact with the N-methyl-D-aspartate (NMDA) receptors. Here we investigated in a comparative way the pro-oxidative effects of quinolinic acid (QA) and malonate, two neurotoxic substances that act through distinct primary molecular mechanisms on the production of thiobarbituric acid reactive species (TBARS) by brain homogenates. In fact, QA is thought to activate directly the NMDA receptor, whereas malonate seems to act primarily by inhibiting oxidative metabolism. The malonate-induced TBARS formation was not modified by cyanide (CN-) or 2,4-dinitrophenol. MK-801 did not reduce basal or malonate induced-TBARS production in fresh tissues preparations. However, in heat-treated preparations a significant effect of MK-801 against basal TBARS production was observed, but not on the malonate induced-TBARS production. QA induced-TBARS production was significantly prevented by MK-801 either in fresh or heat-treated preparations. The antioxidant effect of MK-801 on basal and QA-induced TBARS production increased as the temperatures used to treat S1 were increased. Succinate dehydrogenase (SDH) was inhibited by malonate but not by QA. Malonate was able to chelate iron(II) and the malonate-iron complex(es) is(are) active as measured by its(their) activity on deoxyribose degradation assay. These findings indicate that direct interactions of malonate with NMDA receptors are not involved in malonate pro-oxidative activity in vitro. QA pro-oxidative activity in vitro was related, at least in part, to its capability in stimulate NMDA receptors. Taken together, these findings indicated that malonate pro-oxidative activity in vitro could be attributed to its capability of changing the ratio Fe2+/Fe3+, which is essential to TBARS production.

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Effect of quinolinic acid on endogenous antioxidants in rat corpus striatum

Cited by 111 publications

References 15 publications

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Metabolic changes in quinolinic acid‐lesioned rat striatum detected non‐invasively by in vivo ¹H NMR spectroscopy

N-methyl-D-aspartate Receptors are Involved in the Quinolinic Acid, but not in the Malonate Pro-oxidative Activity in vitro

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Effect of quinolinic acid on endogenous antioxidants in rat corpus striatum

Cited by 111 publications

References 15 publications

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Effect of caffeic acid and rofecoxib and their combination against intrastriatal quinolinic acid induced oxidative damage, mitochondrial and histological alterations in rats

Metabolic changes in quinolinic acid‐lesioned rat striatum detected non‐invasively by in vivo 1H NMR spectroscopy

N-methyl-D-aspartate Receptors are Involved in the Quinolinic Acid, but not in the Malonate Pro-oxidative Activity in vitro

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Metabolic changes in quinolinic acid‐lesioned rat striatum detected non‐invasively by in vivo ¹H NMR spectroscopy