Vitamin E attenuates the toxic effects of intrastriatal injection of 6-hydroxydopamine (6-OHDA) in rats: Behavioral and biochemical evidence

Cadet, Jean Lud; Katz, M; Jackson‐Lewis, Vernice; Fahn, Stanley

doi:10.1016/0006-8993(89)91530-8

Cited by 151 publications

(53 citation statements)

References 25 publications

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“…8,9,23) Eugenol is an essential oil constituent extracted from cloves and used as a food flavouring agent, and was reported to have antioxidant activity. [10][11][12] In this study, we examined the effect of eugenol against 6-OHDA neurotoxicity by measuring decreases of DA, DOPAC, and HVA as markers of dopaminergic neuronal injury.…”

Section: Discussionmentioning

confidence: 99%

Eugenol [2-Methoxy-4-(2-propenyl)phenol] Prevents 6-Hydroxydopamine-Induced Dopamine Depression and Lipid Peroxidation Inductivity in Mouse Striatum

Kabuto

Tada

Kohno

2007

Biological & Pharmaceutical Bulletin

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Section: Discussionmentioning

confidence: 99%

Eugenol [2-Methoxy-4-(2-propenyl)phenol] Prevents 6-Hydroxydopamine-Induced Dopamine Depression and Lipid Peroxidation Inductivity in Mouse Striatum

Kabuto

Tada

Kohno

2007

Biological & Pharmaceutical Bulletin

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“…In this regard, a variety of antioxidants were applied in both in vivo and in vitro for the prevention of 6-OHDA-induced oxidative damage. 21,24 Recently, antioxidative effects of melatonin, the pineal hormone, have also been shown both in vivo and in vitro. 11,12,24 The current demonstration that 6-OHDA-induced increases MDA return to normal following melatonin treatment also support a role for melatonin as an antioxidant, possibly by scavenging free radicals.…”

Section: Discussionmentioning

confidence: 99%

Melatonin increases striatal dopaminergic function in 6-OHDA-lesioned rats

et al. 1998

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“…Inhibition of complex I by paraquat also leads to the formation of superoxide radicals (Turrens and Boveris, 1980). The partial, or even complete, prevention of the neurotoxic effects of 6-OHDA and iron by prior administration of iron chelating agents , vitamin E (Cadet et al, 1989;Perumal et al, 1992) and the MAO-B inhibitor selegiline (Knoll, 1986) may also be regarded as indirect evidence for the formation of free radicals.…”

Section: Behavioural Changes After Unilateral Lesionsmentioning

confidence: 98%

Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man

Gerlach

Riederer

1996

J. Neural Transmission

443

221

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Animal models are an important aid in experimental medical science because they enable one to study the pathogenetic mechanisms and the therapeutic principles of treating the functional disturbances (symptoms) of human diseases. Once the causative mechanism is understood, animal models are also helpful in the development of therapeutic approaches exploiting this understanding. On the basis of experimental and clinical findings. Parkinson's disease (PD) became the first neurological disease to be treated palliatively by neurotransmitter replacement therapy. The pathological hallmark of PD is a specific degeneration of nigral and other pigmented brainstem nuclei, with a characteristic inclusion, the Lewy body, in remaining nerve cells. There is now a lot of evidence that degeneration of the dopaminergic nigral neurones and the resulting striatal dopamine-deficiency syndrome are responsible for its classic motor symptoms akinesia and bradykinesia. PD is one of many human diseases which do not appear to have spontaneously arisen in animals. The characteristic features of the disease can however be more or less faithfully imitated in animals through the administration of various neurotoxic agents and drugs disturbing the dopaminergic neurotransmission. The cause of chronic nigral cell death in PD and the underlying mechanisms remain elusive. The partial elucidation of the processes underlie the selective action of neurotoxic substances such as 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), has however revealed possible molecular mechanisms that give rise to neuronal death. Accordingly, hypotheses concerning the mechanisms of these neurotoxines have been related to the pathogenesis of nigral cell death in PD. The present contribution starts out by describing some of the clinical, pathological and neurochemical phenomena of PD. The currently most important animal models (e.g. the reserpine model, neuroleptic-induced catalepsy, tremor models, experimentally-induced degeneration of nigrostriatal dopaminergic neurons with 6-OHDA, methamphetamine, MPTP, MPP+, tetrahydroisoquinolines, beta-carbolines, and iron) critically reviewed next, and are compared with the characteristic features of the disease in man.

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Vitamin E attenuates the toxic effects of intrastriatal injection of 6-hydroxydopamine (6-OHDA) in rats: Behavioral and biochemical evidence

Cited by 151 publications

References 25 publications

Eugenol [2-Methoxy-4-(2-propenyl)phenol] Prevents 6-Hydroxydopamine-Induced Dopamine Depression and Lipid Peroxidation Inductivity in Mouse Striatum

Eugenol [2-Methoxy-4-(2-propenyl)phenol] Prevents 6-Hydroxydopamine-Induced Dopamine Depression and Lipid Peroxidation Inductivity in Mouse Striatum

Melatonin increases striatal dopaminergic function in 6-OHDA-lesioned rats

Animal models of Parkinson's disease: An empirical comparison with the phenomenology of the disease in man

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