Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0030567 (Parkinson's disease)
 63,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Membrane lipid peroxidation has been suggested to participate in the nigral degeneration of Parkinson's disease. In the present study, we demonstrate that bromocriptine inhibits lipid peroxidation in phospholipid liposomes induced by dopa and iron complexes. Because this lipid peroxidation is not mediated by active oxygen species, antioxidant properties of bromocriptine do not seem to be derived from radical scavenging effects in our experimental conditions. Bromocriptine had no scavenging effect on superoxide produced by hypoxanthine-xanthine oxidase when determined by the chemiluminescence assay using MCLA, a Cypridina luciferin analog, as a probe.
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PMID:Inhibitory effects of bromocriptine on phospholipid peroxidation induced by dopa and iron. 774 68

Bromocriptine, a dopamine D2 receptor agonist, has widely been used for patients with Parkinson's disease. In this study, we examined its neuroprotective effects against neuronal damage in the CA1 subfield of the hippocampus following experimental cerebral ischemia in the Mongolian gerbil. Forebrain ischemia was induced by occlusion of bilateral common carotid arteries for 3 min. Bromocriptine, at a dose of 0.3 or 3 mg/kg, was injected i.p. 30 min before the onset of ischemia. Histopathological observations showed that neuronal damage to hippocampal CA1 neurons, which was seen 7 days after ischemia in vehicle-treated animals, was prevented by bromocriptine treatment. Immunohistochemical staining for copper/zinc superoxide dismutase and manganese superoxide dismutase decreased markedly in the CA1 neurons of vehicle-treated animals 2 days after ischemia when histological neuronal destruction was not yet seen, but was well preserved in bromocriptine-treated animals. The present findings show that bromocriptine protects against ischemia-induced neuronal damage, and that the mechanism of the neuroprotection may relate to the preservation of SODs. Bromocriptine, which was recently shown to be a potent free radical scavenger, may have a potent neuroprotective action against disorders including ischemic stroke.
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PMID:Bromocriptine protects against delayed neuronal death of hippocampal neurons following cerebral ischemia in the gerbil. 775 51

A 64-year-old man was diagnosed to have Parkinson's disease when aged 42 years and since then has been treated with levodopa and benserazide (up to 875 mg daily). Bromocriptine (up to 35 mg daily) was added to the medication 9 years ago. 3 1/2 years ago he developed exertional dyspnoea (NYHA class II-III) and lost 5 kg in weight. Chest radiography demonstrated pleural effusion and interstitial pulmonary changes in both lung bases. Erythrocyte sedimentation rate was 37 mm in the first hour and the white cell count 10,400/microliters. Extensive tests failed to find malignant tumour or any infectious-inflammatory condition. As it was suspected that the pleuropulmonary changes were associated with the bromocriptine intake, it was discontinued and biperiden and selegiline substituted for it. The pleural effusion regressed almost completely within 8 weeks, and the laboratory tests pointing to inflammation disappeared completely. Clinical, biochemical and radiological tests have remained normal for the last 3 years. The clinical course makes a causal relationship between bromocriptine intake and the pleuropulmonary changes highly probable.
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PMID:[Bromocriptine-induced pleuropneumopathy]. 795 89

It has been suggested that free radicals may adversely influence the pathogenesis of Parkinson's disease. We conducted this study to determine whether bromocriptine, an agent widely used for treating parkinsonism, possesses antioxidant effects. Bromocriptine scavenged superoxide produced from a superoxide generating system (hypoxanthine-xanthine oxidase) by the spin-trapping method using electron spin resonance. Bromocriptine had a strong scavenging effect on the 5,5-dimethyl-1-pyrroline-N-oxide hydroxide signal produced from Fenton's reaction. Bromocriptine also attenuated the stable free radical diphenyl-p-picrylhydrazyl signal. This drug inhibited the autooxidation of rat brain homogenates in a dose-dependent manner in vitro. Autooxidation of brain homogenates collected from rats treated with bromocriptine (2.5 mg/kg, i.p., daily for 3 days) was significantly reduced as compared with values in untreated rat homogenates. These observations suggest that bromocriptine is a free radical scavenger and a potent antioxidant.
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PMID:Antioxidant properties of bromocriptine, a dopamine agonist. 811 89

Pleurisy of initially unknown origin was found in a patient who was treated with bromocriptine for Parkinson's disease for 6 years. At presentation, bilateral pleural thickening existed that caused severe restriction of pulmonary function. There were an elevated erythrocyte sedimentation rate, polyclonal hypergammaglobulinaemia, increased levels of acute phase proteins and anaemia. After withdrawal of the bromocriptine the patient's complaints as well as the laboratory parameters markedly improved. Further loss of pulmonary function did not occur. However, the pleural thickening did not resolve, not even upon subsequent corticosteroid treatment, probably due to fibrosis. Together, these findings strongly suggest a causative role of bromocriptine. The results of the laboratory studies suggested an immunopathogenetic mechanism, but in vitro lymphocyte-proliferation studies and skin patch tests with bromocriptine were negative. Bromocriptine should be considered as a cause of pleurisy. The drug must be stopped immediately upon the occurrence of pleural thickening in order to prevent impairment of pulmonary function. In addition, periodic laboratory and X-ray studies in patients on long-term bromocriptine treatment should be considered.
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PMID:Suggestive evidence for bromocriptine-induced pleurisy. 871 45

Bromocriptine, a dopamine agonist, alleviates symptoms of Parkinson's disease, even when administered alone, and is used for its treatment. Better therapeutic effects are, however, achieved when bromocriptine is used in combination with levodopa. In this study, we examined the biochemical changes caused by bromocriptine administration with and without levodopa, and evaluated the effects of the treatments on dopamine turnover in the mouse striatum. Results show that dopamine turnover is suppressed by the administration of bromocriptine alone with a slight decrease in the amount of dopamine, and dopamine turnover is very strongly promoted by the administration of levodopa. When the two drugs are administered together, bromocriptine enhances the levodopa-induced increase in dopamine turnover in the striatum. These findings indicate that bromocriptine therapy in combination with levodopa enhances the dopaminergic function and suggest that the combination therapy of bromocriptine and levodopa shows good efficacy. The results of this study may, thus, provide a theoretical basis for the combination therapy of bromocriptine and levodopa.
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PMID:Effects of bromocriptine on dopamine turnover with or without levodopa. 872 88

In this Danish-Norwegian randomized double-blind parallel-group multicentre study, we compared the therapeutic response of slow-release Madopar HBS to standard Madopar in 134 de novo patients with idiopathic Parkinson's disease during a 5-year period. The drugs were dosed according to the individual need of the patients. The Webster, NUDS, UPDRS and Hoehn & Yahr scales were used for evaluation of symptoms. Addition of a morning dose of standard Madopar 62.5 mg was allowed after 6 months. Bromocriptine could be administered but not Selegiline. Sixty-five patients got Madopar HBS and 69 standard Madopar. Surprisingly, no differences were found as to the mean daily levodopa dose, the mean number of daily doses or the use of the doses of bromocriptine. Unexpectedly, we found a trend towards a more frequent use of a morning dose of standard Madopar in the group treated with the standard formulation. No differences were observed in the occurrence of motor fluctuations or dyskinesia, the incidence of which was relatively low. Sustained-release Madopar (HBS) thus proved to be as effective as standard Madopar in the long-term treatment of de novo parkinsonian patients, but the drug showed no advantage in postponing or reducing the long-term levodopa treatment problems.
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PMID:Sustained-release Madopar HBS compared with standard Madopar in the long-term treatment of de novo parkinsonian patients. 882 66

Parkinson's disease (PD) is the second most common neurodegenerative disorder worldwide and is characterised by cardinal clinical features and specific pathological findings. It is possible to detect PD early on in the course of the disease, and certain laboratory studies may identify preclinical stages. Based on this information, and the hypothesis that there is a long preclinical period, there appears to be a window of opportunity to influence the natural course of the disease. Postulates regarding pathogenesis, such as oxidative stress and excitotoxicity, have led to the discovery of abnormal mitochondrial function in PD and a search for biochemical markers. Functional imaging studies have detected subclinical nigral dopaminergic dysfunction in individuals at risk of developing PD. Current symptomatic therapies are aimed at enhancing dopaminergic transmission. However, some commonly used PD medications may have alternative actions with both symptomatic and neuroprotective consequences. Bromocriptine has been postulated to have antioxidant effects and amantadine to have N-methyl-D-aspartate (NMDA) receptor antagonistic properties. Both have been reported to be associated with improved survival in PD. Additionally, monoamine oxidase type B inhibitors may provide neuroprotection. Recent new medications are also under study with regard to neuroprotection. Despite these advances, until there is a better understanding of the aetiology and pathogenesis of PD, there will be no definitive long-term benefit of early diagnosis and treatment of PD.
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PMID:Early detection of Parkinson's disease. Implications for treatment. 887 10

High doses of bromocriptine used for treatment of Parkinson's disease may be associated with pleuropulmonary complications. Isolated pleural effusions are a rare manifestation as is lower limbs edema are an exceptionally one. We report the case of a 67-year-old man, treated since five years by a daily dose of 30 mg of bromocriptine for Parkinson's disease, who developed important leg's edema and a few months later an exsudative right pleural effusion. No etiologies were found. Bromocriptine was discontinued. The evolution was characterized by nearly complete resolution of pleural effusion and disparition of lower limbs edema.
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PMID:[Pleural effusion and severe edema of the lower limbs induced by bromocriptine]. 888 Nov 98

The involvement of abdominal afferent vagal activity and serotonergic mechanisms were examined following intravenous administration of talipexole, a dopamine D2 receptor agonist used for treatment of Parkinson's disease, in anesthetized rats. Intravenous administration of dopamine receptor agonists including D1/D2 components increased the spontaneous firing of afferent vagal neurons as did 2-methyl-5-hydroxytryptamine. Both talipexole (0.25-1.0 mg/kg) and bromocriptine (1.0-10.0 mg/kg) increased vagal nerve activity in a dose-dependent manner, and the effect of 10 mg/kg of bromocriptine was significantly greater than that noted with 1.0 mg/kg of talipexole. Increasing vagal firing induced by talipexole was prevented by pretreatment with granisetron, but not with metoclopramide or by spinal section, indicating that afferent vagal firing was mediated via stimulation of the 5-HT3 receptors on the neurons and secondarily caused by stimulation of dopamine receptors. On the other hand, bromocriptine at 5 mg/kg increased 5-HIAA concentration in the ileum, and serotonin turnover (5-HIAA/5-HT) was increased approximately 4-fold when compared to the vehicle group. Bromocriptine also increased the activities of tryptophan hydroxylase and monoamine oxidase. Talipexole at 0.5 mg/kg did not affect ileal 5-HT metabolism and the enzymatic activities. These findings suggest that dopamine receptor agonists may induce changes in abdominal afferent vagal activity and ileal 5-HT metabolism similar to those observed with emetic compounds, and that talipexole has a much smaller influence on serotonin-mediated responses than does bromocriptine with equipotent antiparkinsonian doses. One of the possible reason why talipexole showed fewer emetic side effects in patients with Parkinson's disease may be that the emetic responses triggered by D2 receptor stimulation may secondarily cause an increase of abdominal afferent vagal activity, which may be weakened by the 5-HT3 receptor antagonistic property of talipexole.
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PMID:Effects of talipexole on emesis-related changes in abdominal afferent vagal activity and ileal serotonin metabolism in rats. 905 50


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