Free radical scavenging properties of apomorphine enantiomers and dopamine: Possible implication in their mechanism of action in parkinsonism

Sam, E.; Verbeke, Norbert

doi:10.1007/bf02251227

Cited by 43 publications

(22 citation statements)

References 41 publications

(34 reference statements)

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“…The S-apomorphine, which is not a dopamine agonist, possesses the same radical scavenging and neuroprotective properties in these systems. 14,15,33 Our findings are in line with a recently reported observation that bromocriptine, a DA agonist, reversed the MPTP-induced hydroxyl radical formation in substantia nigra and striatum as well as striatal DA depletion in mice. 19 The relatively high doses (5 and 10 mg/kg) of APO used in this study to achieve neuroprotection relates to the pharmacokinetically unstable and readily oxidizable nature of APO.…”

Section: Discussionsupporting

confidence: 81%

Apomorphine protects against MPTP-induced neurotoxicity in mice

et al. 1999

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Section: Discussionsupporting

confidence: 81%

Apomorphine protects against MPTP-induced neurotoxicity in mice

et al. 1999

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“…For example, bromocriptine and apomorphine act as free radical scavengers (Yoshikawa et al, 1994;Sam and Verbeke, 1995;Gr€ unblatt et al, 1999). Dopamine D3 receptors are not critical for the neuroprotection by the D3 agonist pramipexole, in 3-acetylpyridine-treated rats (Sethy et al, 1997), and pramipexole itself may possess significant intrinsic antioxidant properties (Hall et al, 1996;Ling et al, 1999).…”

Section: Discussionmentioning

confidence: 94%

Dopamine D2 and D3 receptor agonists limit oligodendrocyte injury caused by glutamate oxidative stress and oxygen/glucose deprivation

Rosin

Colombo

Calver

et al. 2005

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Dopamine receptor activation is thought to contribute adversely to several neuropathological disorders, including Parkinson's disease and schizophrenia. In addition, dopamine may have a neuroprotective role: dopamine receptor agonists are reported to protect nerve cells by virtue of their antioxidant properties as well as by receptor-mediated mechanisms. White matter injury can also be a significant factor in neurological disorders. Using real-time RT-PCR, we show that differentiated rat cortical oligodendrocytes express dopamine D2 receptor and D3 receptor mRNA. Oligodendrocytes were vulnerable to oxidative glutamate toxicity and to oxygen/glucose deprivation injury. Agonists for dopamine D2 and D3 receptors provided significant protection of oligodendrocytes against these two forms of injury, and the protective effect was diminished by D2 and D3 antagonists. Levels of oligodendrocyte D2 receptor and D3 receptor protein, as measured by Western blotting, appeared to increase following combined oxygen and glucose deprivation. Our results suggest that dopamine D2 and D3 receptor activation may play an important role in oligodendrocyte protection against oxidative glutamate toxicity and oxygen-glucose deprivation injury.

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“…It has also been reported that dopamine receptor agonists have neuroprotective effects that are caused by nonreceptor-mediated mechanisms. For example, bromocriptine and apomorphine act as free radical scavengers (Yoshikawa et al, 1994;Sam and Verbeke, 1995;Grünblatt et al, 1999). In addition, dopamine D3 receptors are not critical for the neuroprotection by the D3 agonist, pramipexole, in 3-acetyl pyridine-treated rats (Sethy et al, 1997).…”

mentioning

confidence: 99%

The Activation of Dopamine D4 Receptors Inhibits Oxidative Stress-Induced Nerve Cell Death

et al. 2001

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Oxidative stress is thought to be the cause of nerve cell death in many CNS pathologies, including ischemia, trauma, and neurodegenerative disease. Glutamate kills nerve cells that lack ionotropic glutamate receptors via the inhibition of the cystineglutamate antiporter x c Ϫ , resulting in the inhibition of cystine uptake, the loss of glutathione, and the initiation of an oxidative stress cell death pathway. A number of catecholamines were found to block this pathway. Specifically, dopamine and related ligands inhibit glutamate-induced cell death in both clonal nerve cell lines and rat cortical neurons. The protective effects of dopamine, apomorphine, and apocodeine, but not epinephrine and norepinephrine, are antagonized by dopamine D4 antagonists. A dopamine D4 agonist also protects, and this protective effect is inhibited by U101958, a dopamine D4 antagonist. Although the protective effects of some of the catecholamines are correlated with their antioxidant activities, there is no correlation between the protective and antioxidant activities of several other ligands. Normally, glutamate causes an increase in reactive oxygen species (ROS) and intracellular Ca 2ϩ . Apomorphine partially inhibits glutamate-induced ROS production and blocks the opening of cGMP-operated Ca 2ϩ channels that lead to Ca 2ϩ elevation in the late part of the cell death pathway. These data suggest that the protective effects of apomorphine on oxidative stress-induced cell death are, at least in part, mediated by dopamine D4 receptors via the regulation of cGMP-operated Ca 2ϩ channels.

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Free radical scavenging properties of apomorphine enantiomers and dopamine: Possible implication in their mechanism of action in parkinsonism

Cited by 43 publications

References 41 publications

Apomorphine protects against MPTP-induced neurotoxicity in mice

Apomorphine protects against MPTP-induced neurotoxicity in mice

Dopamine D2 and D3 receptor agonists limit oligodendrocyte injury caused by glutamate oxidative stress and oxygen/glucose deprivation

The Activation of Dopamine D4 Receptors Inhibits Oxidative Stress-Induced Nerve Cell Death

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