Vitamin E attenuates reserpine-induced oral dyskinesia and striatal oxidized glutathione/reduced glutathione ratio (GSSG/GSH) enhancement in rats

Abı́lio, Vanessa C.; Araujo, Carlos C.S.; Bergamo, Marcelo; Calvente, Patricia R.V.; D’Almeida, Vânia; Ribeiro, R. de A.; Frussa‐Filho, Roberto

doi:10.1016/s0278-5846(02)00340-8

Cited by 67 publications

(36 citation statements)

References 38 publications

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“…The resulting increase in oxidative activity provokes an increase in circulating levels of SOD as a protective response, as has been described in patients with TD [11]. Preliminary data supports the use of antioxidants in reversing and/or treating TD [25,26,44], which has raised hopes that these agents may be useful in protecting against the later development of TD in patients who need to receive neuroleptics, viz. the treatment of schizophrenia.…”

Section: Discussionmentioning

confidence: 59%

Effect of Chronic N-Acetyl Cysteine Administration on Oxidative Status in the Presence and Absence of Induced Oxidative Stress in Rat Striatum

et al. 2007

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Antioxidants have possible therapeutic value in neurodegenerative disorders, although they may have pro-oxidant effects under certain conditions. Glutathione (GSH) is a key free radical scavenger. N-acetylcysteine (NAC) bolsters GSH and intracellular cysteine and also has effective free radical scavenger properties. The effects of chronic NAC administration (50 mg/kg/day, 500 mg/kg/day, 1500 mg/kg/day x 21 days) on cellular markers of oxidative status was studied in striatum of healthy male Sprague-Dawley rats as well as in animals with apparent striatal oxidative stress following chronic haloperidol treatment (1.5 mg/kg/day x 3 weeks). In non-haloperidol treated animals, NAC 50 and 500 mg/kg did not affect oxidative status, although NAC 1,500 mg/kg significantly increased striatal superoxide levels, decreased lipid peroxidation and increased consumption of reduced glutathione (GSH). Haloperidol alone evoked a significant increase in superoxide and lipid peroxidation. All NAC doses blocked haloperidol induced increases in superoxide levels, while NAC 500 mg/kg and 1,500 mg/kg prevented haloperidol-associated lipid peroxidation levels and also increased the GSSG/GSH ratio. NAC may protect against conditions of striatal oxidative stress, although possible pro-oxidative actions at high doses in otherwise healthy individuals, e.g. to offset worsening of neurodegenerative illness, should be viewed with caution.

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Section: Discussionmentioning

confidence: 59%

Effect of Chronic N-Acetyl Cysteine Administration on Oxidative Status in the Presence and Absence of Induced Oxidative Stress in Rat Striatum

et al. 2007

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“…Chronic reserpine treatment also significantly decreased reduced glutathione, an endogenous antioxidant and cellular antioxidant enzymes superoxide dismutase and catalase levels, further supporting the involvement of free radical toxicity in reserpine-induced orofacial dyskinesia. Other investigators have also demonstrated that reserpine-induced oral dyskinesia is closely associated with the oxidative stress process (Calvente et al, 2002;Abilio et al, 2003;Burger et al, 2003). Sussman et al (1997) reported that it is possible that reserpine-induced orofacial dyskinesia may be initiated by altered striatal dopaminergic function, but the persistent neuropathological changes involve GABAergic efferent to striatal dopamine.…”

Section: Discussionmentioning

confidence: 99%

Effect of Withania somnifera root extract on reserpine‐induced orofacial dyskinesia and cognitive dysfunction

Naidu

Singh

Kulkarni

2006

Phytotherapy Research

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Tardive dyskinesia is one of the major side effects of long-term neuroleptic treatment. The pathophysiology of this disabling and commonly irreversible movement disorder is still obscure. Vacuous chewing movements in rats are widely accepted as an animal model of tardive dyskinesia. Oxidative stress and products of lipid peroxidation are implicated in the pathophysiology of tardive dyskinesia. Repeated treatment with reserpine (1.0 mg/kg) on alternate days for a period of 5 days (days 1, 3 and 5) significantly induced vacuous chewing movements and tongue protrusions in rats. Chronic treatment with Withania somnifera root extract (Ws) for a period of 4 weeks to reserpine treated animals significantly and dose dependently (50 and 100 mg/kg) reduced the reserpine-induced vacuous chewing movements and tongue protrusions. Reserpine treated animals also showed poor retention of memory in the elevated plus maze task paradigm. Chronic Ws administration significantly reversed reserpine-induced retention deficits. Biochemical analysis revealed that chronic reserpine treatment significantly induced lipid peroxidation and decreased the glutathione (GSH) levels in the brains of rats. Chronic reserpine treated rats showed decreased levels of antioxidant defense enzymes, superoxide dismutase (SOD) and catalase. Chronic administration of Ws root extract dose dependently (50 and 100 mg/kg) and significantly reduced the lipid peroxidation and restored the decreased glutathione levels by chronic reserpine treatment. It also significantly reversed the reserpine-induced decrease in brain SOD and catalase levels in rats. The major findings of the present study indicate that oxidative stress might play an important role in the pathophysiology of reserpine-induced abnormal oral movements. In conclusion, Withania somnifera root extract could be a useful drug for the treatment of drug-induced dyskinesia.

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“…Conversely, the protocol used here (repeated treatment with a low dose) reduced tyrosine hydroxylase staining in the substantia nigra and striatum, and part of the alterations induced by the treatment were not recovered after 30 days of treatment withdrawal [8]. Second, it has been shown that reserpine treatment increases brain oxidative stress and this alteration is accompanied by behavioral deficits [10,22,23]. In addition, in a previous study [9] the repeated treatment with a low dose of reserpine induced an increase in striatal level of lipid peroxidation, which occurred concomitantly to the motor impairment.…”

Section: Discussionmentioning

confidence: 82%

“…blockage of the vesicular transport of monoamines), there is clear evidence that reserpine also causes an increase in cellular oxidative stress, possibly potentiated by the rise in the levels of dopamine in the cytoplasm, which undergoes oxidative metabolism [10]. In this respect, the central nervous system is quite vulnerable to reactive oxygen species (ROS), which play a very important function in the pathogenesis of neurodegenerative disorders, including PD [11].…”

Section: Introductionmentioning

confidence: 99%

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

Sarmento-Silva¹,

Lima²,

Cabral³

et al. 2015

Biochem Pharmacol (Los Angel)

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Vitamin E attenuates reserpine-induced oral dyskinesia and striatal oxidized glutathione/reduced glutathione ratio (GSSG/GSH) enhancement in rats

Cited by 67 publications

References 38 publications

Effect of Chronic N-Acetyl Cysteine Administration on Oxidative Status in the Presence and Absence of Induced Oxidative Stress in Rat Striatum

Effect of Chronic N-Acetyl Cysteine Administration on Oxidative Status in the Presence and Absence of Induced Oxidative Stress in Rat Striatum

Effect of Withania somnifera root extract on reserpine‐induced orofacial dyskinesia and cognitive dysfunction

Alpha-Tocopherol Counteracts Cognitive and Motor Deficits Induced by Repeated Treatment with Reserpine

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