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PubMed1991

Central action of benserazide after COMT inhibition demonstrated in vivo by PET.

Positron emission tomography (PET) following intravenous administration of beta-[11C]-L-DOPA provides a method of assessing regional cerebral uptake and utilization of levodopa. Cerebral levodopa kinetics in the rhesus monkey were investigated after the inhibition of catechol-O-methyltransferase (COMT) with RO 40-7592, and after coadministration of the peripheral aromatic L-amino acid decarboxylase (AADC) inhibitors benserazide and carbidopa. Pretreatment with RO 40-7592 (10 mg/kg), benserazide (10 mg/kg) or carbidopa (3.5 mg/kg) did not change striatal k3, which mainly reflects the ability for the brain tissue to convert [11C]-L-DOPA to [11 C]-dopamine, although the brain's uptake of radioactivity increased substantially after pretreatment with the AADC inhibitors. When benserazide was coadministered with RO 40-7592 (10 mg/kg) a dose-dependent decrease in striatal k3 was measured with an apparent ED50 of 3 mg/kg. No such effect was indicated after pretreatment with the combination of RO 40-7592 (10 mg/kg) and carbidopa (3.5 mg/kg). The possible negative interactions of coadministration with COMT inhibitors and predominantly peripherally acting AADC inhibitors must be considered when used in the therapy of Parkinson's disease.

Animals↗

PubMed1982

Effect of benserazide on the levels of pineal 5-hydroxytryptamine, melatonin synthesising enzymes and serum melatonin.

The effect of benserazide, an aromatic L-amino acid decarboxylase inhibitor, has been investigated on pineal 5-hydroxytryptamine content, melatonin synthesising enzyme activities and serum melatonin concn. Increasing doses of benserazide caused increasing reductions in the pineal content of 5-hydroxytryptamine. Dark phase serum melatonin concns were also greatly reduced. The drug abolished the diurnal rhythm of hydroxyindole-O-methyltransferase by increasing the light period activities and decreasing the night levels of this enzyme. Pineal N-acetyltransferase was unaffected. It is concluded that benserazide probably inhibits melatonin synthesis by preventing the formation of the substrate, 5-hydroxytryptamine.

Acetylserotonin O-Methyltransferase↗

PubMed1986

Effect of benserazid and 6-hydroxydopamine on the development of the last larval instar of the house cricket, Acheta domestica L.

The effect of benserazid and 6-OHDA on the duration of the last larval instar and development of wings with intact corpora allata and following allatectomy on Acheta domestica L. was studied. 6-OHDA failed to alter the duration of the last larval instar in the nymphs with intact corpora allata but prolonged it in the allatectomized crickets. Introduction of 6-OHDA in the second phase of the last larval instar caused a deformation of the wings both in allatectomized and intact crickets. Injection of benserazid to the nymphs of the last larval instar prolonged the duration of this phase only in the presence of the corpora allata. The effect of benserazid can be connected to elimination of central inhibition of the corpora allata involving dopaminergic neurons of the brain.

Animals↗

PubMed1980

The influence of benserazide on changes in monoamine oxidase activity in some rat tissues following treatment with L-DOPA.

1. This study was designed to see whether or not increases in monoamine oxidase (MAO) specific activity that follow chronic treatment of rats with L-dihydroxyphenylalanine (L-DOPA) could be modified by benserazide (Ro 4-4602), an inhibitor of L-aromatic amino acid decarboxylase, and to compare the properties of the increased MAO activity with those of control animals. 2. Male wistar rats were treated with L-DOPA (250 mg/kg) and benserazide (40 mg/kg) either alone or in combination for 10 days. 3. The activity of MAO in homogenates of heart, kidney, liver and brain was measured with 5-hydroxytryptamine (5-HT) and benzylamine (BZ). 4. The significant increases in MAO specific activity seen in heart and kidney following L-DOPA treatment could be reduced or prevented by benserazide. 5. Use of the selective MAO inhibitor clorgyline showed that the increases in MAO specific activity, when measured with either 5-HT or BZ were due to an increase in the number of active centres of MAO-A, in the rat heart. 6. There was a significant increase in the Vmax of the enzyme reaction with 5-HT, in the rat heart and kidney homogenates. 7. It is concluded that L-DOPA increases the specific activity of MAO-A in rat heart and kidney as a result of its decarboxylation.

Animals↗

PubMed1977

A controlled study of a dopa decarboxylase inhibitor (benserazide) in the treatment of schizophrenic patients.

In a double-blind controlled study lasting 6 weeks, 32 schizophrenic patients were randomly assigned to one of two treatments: chlorpromazine or benserazide, a dopa decarboxylase inhibitor. Results on each measure were subject to multifactorial analysis of covariance. Benserazide did not appear to be as effective an antipsychotic medicaiton as chlorpromazine. In fact, chlorpromazine was significantly better on measures of tension, excitement, hallucinatory behavior, thinking disturbance, social interest, and drop-out rate. At the relatively low dosages used in this study, it would seem that benserazide had little effect on the cerebral dopa decarboxylase, and it would be worthwhile trying higher dosages.

Adult↗

PubMed1985

Benserazide effects on growth hormone, prolactin, and thyrotropin in normal and acromegalic man.

The effect of benserazide administration on the secretion of GH, PRL, and TSH has been considered as an index of dopamine regulatory actions. Nine acromegalic patients and nine normal subjects were given a single 125 mg oral dose of benserazide, and serum GH, PRL, and TSH were determined by RIA methods every 30 min for 4 h. Benserazide did not alter GH values either in normal subjects or in acromegalic patients. A significant increase of serum PRL was found in both groups, and the increase was similar in normoprolactinemic and in hyperprolactinemic acromegalic patients. A significant increase in TSH levels was found only in acromegalic patients. Thus, a decrease in dopamine outside the blood-brain barrier did not affect GH secretion, whereas PRL secretion was changed in the acromegalic as well as in the control group.

Acromegaly↗

PubMed1979

Levodopa with benserazide or carbidopa in Parkinson disease.

Plasma levodopa and therapeutic responses to treatment with levodopa in combination with benserazide or carbidopa were studied in 49 patients with Parkinson disease not previously treated with levodopa in a blind randomized crossover trial. The treatment periods were 12 weeks; similar dosage schedules were used, with doses that induced equal levels of plasma levodopa in both combinations. In pretrial studies of plasma levodopa responses, 200 mg of levodopa and 50 mg of benserazide was equal to 250 mg of levodopa combined with 25 mg of carbidopa. Equal plasma levodopa responses to both combinations were also found during the trial. There was no significant difference between the treatment groups in beneficial effects on parkinsonian disability and individual symptoms or in the frequency of involuntary movements. However, nausea and vomiting occurred significantly more often during treatment with levodopa and carbidopa than during treatment with levodopa and benserazide. This difference was probably due to inadequate inhibition of peripheral decarboxylase inhibitor by the 1:10 ratio of carbidopa to levodopa.

Benserazide↗

PubMed1979

Study on the reproducibility of human prolactin response to sulpiride, benserazide, insulin hypoglycaemia and arginine infusion.

In order to evaluate the spontaneous variability of prolactin (PRL) release in response to various stimuli applied repeatedly on different occasions, groups of 5 to 12 subjects each underwent consecutive identical tests with one of the following stimuli applied at 3-6 days' intervals: sulpiride (100 mg im), benserazide (50 mg po), insulin hypoglycaemia (0.1 U/kg b. w. iv) and arginine infusion (25 g iv in 30 min). When repeated in the same subjects, arginine and benserazide yielded superimposable results. In contrast to this, insulin hypoglycaemia yielded significantly lower PRL release, while the PRL response to the second sulpiride test was significantly higher than to the first one. When an interval of 10 days was left between two consecutive sulpiride tests, an identical PRL release was observed. These results indicate that arginine and benserazide are reproducible tests for PRL secretion and it is possible that the decreasing effect of insulin hypoglycaemia on PRL release is due to the stressful effect of the stimulus. Finally, sulpiride probably enhances both PRL release and synthesis thus making greater amounts of PRL available to a subsequent stimulus. Since some of the above stimuli are usual tools for the study of the neuroendocrine control of PRL secretion, our findings suggest that caution appears necessary in attributing to any (neuroactive) drug an effect which might be merely due to a lack of reproducibility of the stimulus employed.

Adult↗

PubMed1995

[Benefits of a new galenic form of levodopa and benserazide in the treatment of patients with Parkinson disease].

We describe a new, water-soluble formulation of levodopa plus benserazide (Madopar LIQ) for the treatment of Parkinson's disease. Two dosage strengths are available: 100 mg levodopa plus 25 mg benserazide and 50 mg levodopa plus 12.5 mg benserazide. Pharmacokinetic data show that levodopa absorption is more rapid than with standard Madopar, resulting in a shorter time to peak plasma concentration. Other pharmacokinetic values are comparable to those obtained with the standard formulation. We discuss the clinical advantages of this new water-soluble formulation, particularly when the patient requires rapid onset of action for morning or circadian akinesia. The indications of this formulation in patients with dysphagia and in other clinical situations, e.g. during the postoperative period and for levodopa dosage adjustment in ambulatory care, are discussed.

Aged↗

PubMed1976

[Attempt at potentiation of the action of L-dopa on the secretion of growth hormone by benserazide, disulfiram and propranolol].

Two tests of stimulation of growth hormone secretion were performed in 3 groups of normal children. In the first test L-Dopa was used on its own; in the second, L-Dopa was combined with Benserazide (group A), with Disulfirame (group B), or with Propranolol (group C). In group A the mean peak value after L-Dopa was 9.1 +/- 1.6 ng/ml; with the combination of L-Dopa and Benserazide it was 12.4 +/- 2.4 ng/ml. The difference between the means is not significant. In group B the mean peak value after L-Dopa was 8.9 +/- 3.6 ng/ml; with the combination of L-Dopa and Disulfirame it was 14.5 +/- 4.4 ng/ml. The difference is not significant. In group C the mean peak value after L-Dopa was 9.8 +/- 2.6 ng/ml; with the combination of L-Dopa and Propranolol, it was 10.1 +/- 1.9 ng/ml. Again the difference is not significant. These findings do not provide evidence in favour of the effect of L-Dopa on the secretion of growth hormone being facilitated by an inhibitor of L-Dopa decarboxylase (Benserazide) or of Dopamine beta hydroxylase (Disulfirame), or by a beta blocking agent (Propranolol). The mechanisms of action of L-Dopa and of the various combinations studied are discussed.

Adolescent↗

PubMed2000

Quality control of benserazide-levodopa and carbidopa-levodopa tablets by capillary zone electrophoresis.

In modern practice, the treatment of Parkinson's disease and syndrome is carried out using pharmaceutical formulations containing a combination of levodopa and a decarboxylation inhibitor (carbidopa or benserazide). Two pharmaceutical formulations were quantified by capillary zone electrophoresis using two procedures which differed only in the kind of background electrolyte used. One procedure used a 25 mM phosphate buffer, pH 2.5, while the second one used a 25 mM borate buffer, pH 8.5. The electrophoretic analysis was carried out using an uncoated fused- silica capillary, a separation voltage of 20 kV with currents typically less than 60 microA, and spectrophotometric detection at 205 nm. Calibration curves were performed for levodopa (concentration range 1-100 microg/mL), for carbidopa and benserazide (1-50 microg/mL), and the plots of the peak area versus concentration were found to be linear with a correlation coefficient better than 0.9990. Satisfactory results were obtained when commercial tablets were analyzed in terms of accuracy (98-102%), repeatability (0.6-2.0%), and intermediate precision (1.1-2.6%).

Benserazide↗

PubMed1975

Levodopa alone and in combination with a peripheral decarboxylase inhibitor benserazide (Madopar) in the treatment of Parkinson's disease: A controlled clinical trial.

A combination of levodopa and the extracerebrally acting decarboxylase inhibitor benserazide (ratio 4:1) (Madopar), was compared with levodopa alone in a controlled double-blind clinical multicenter trial on 94 patients with Parkinson's disease. During 4 months of therapy levodopa + benserazide proved superior to levodopa on several accounts. Nausea and vomiting occurred with statistically significant less severity and frequency. Clinical improvement expressed through improvement in Webster rating occurred sooner and was all together greater. The treatment schedules did not differ with regard to other side effects, in particular involuntary movements and reduction in supine blood pressure. Neither treatment seemed to influence liver function, renal function and hematological parameters.

Adult↗

PubMed1983

The effect of l-DOPA and benserazide on the amount of dopamine in the corpus striatum of X-irradiated rats.

The effect of a mixture of l-DOPA and benserazide on the amount of dopamine in the corpus striatum of rats irradiated with 850 R of X-rays was investigated. The amount of dopamine in the corpus striatum was measured fluorimetrically at various times after irradiation. It was found that i.p. administration of l-DOPA and benserazide 1,2 and 5 days after irradiation produces significant replenishment of dopamine in the striatum, thus indicating that precursor uptake and metabolism, and probably amine storage, remained unaltered after irradiation.

Animals↗

PubMed1982

Characteristics and specificity of phenelzine and benserazide as inhibitors of benzylamine oxidase and monoamine oxidase.

The selectivity of benserazide and phenelzine toward inhibition of benzylamine oxidase (BzAO) and monoamine oxidases (MAO-A and MAO-B) was studied in homogenates of rat skull and lung. In addition, the kinetic interaction and reversibility of BzAO inhibition were assessed. Both drugs inhibited BzAO but only phenelzine inhibited MAO, whether tested in vitro or in vivo. Neither compound acted as an irreversible inhibitor of BzAO. Benserazide was found to be a noncompetitive inhibitor. Phenelzine acted as a substrate for BzAO followed by product-induced noncompetitive inhibition which was labile at 37 degrees but not at 4 degrees. A reversible component in phenelzine-induced inhibition of MAO-A and -B is also suggested from in vivo studies.

Animals↗

PubMed1991

Inhibition of tryptophan hydroxylase by benserazide and other catechols.

Tryptophan hydroxylase (L-tryptophan, tetrahydropteridine:oxygen oxidoreductase [5-hydroxylating]; EC 1.14.16.4; TPH), the initial and rate-limiting enzyme in the biosynthesis of the neurotransmitter serotonin, was inhibited directly by benserazide, an inhibitor of aromatic-L-amino-acid decarboxylase (3,4-dihydroxy-L-phenylalanine carboxy-lyase; EC 4.1.1.28; AAAD). Benserazide was a competitive inhibitor for the pterin cofactor tetrahydrobiopterin and an uncompetitive inhibitor for the substrate tryptophan. NSD 1015, another decarboxylase inhibitor, did not directly inhibit TPH. Other compounds with catechol moieties in their structures such as 3,4-dihydroxyphenylalanine (DOPA), dopamine, apomorphine, and SKF 38393 were also found to be potent inhibitors of TPH. These results indicate that drugs or neurotransmitters with catechol structures directly inhibit the activity of TPH and add to a growing body of evidence indicating that endogenous dopamine can exert untoward effects on serotonin neurons, including inhibition of TPH. Furthermore, the use of decarboxylase inhibitors to cause the accumulation of 5-hydroxytryptophan as an in vivo measure of TPH activity could be problematic, particularly when drugs with catechol structures or dopamine-releasing compounds are also administered.

2,3,4,5-Tetrahydro-7,8-dihydroxy-1-phenyl-1H-3-ben↗

PubMed1976

Comparison of levodopa with carbidopa or benserazide in parkinsonism.

The therapeutic efficacy and side-effects of two preparations of levodopa with extracerebral decarboxylase inhibitors have been compared in 19 patients with idiopathic parkinsonism in a blind randomised crossover trial. The mean daily dose of levodopa was 658 +/- 64 mg/day (mean +/- S.E.M.) when given together with carbidopa 66 mg/day and 605 +/- 59 mg/day when levodopa was combined with benserazide 151 mg/day. There was no significant difference between the treatment regimens either in beneficial effects on parkinsonian symptoms and signs or in the adverse effects of levodopa assessed by a clinical observer unaware of the treatment given. Of the 19 patients studied, 9 preferred the carbidopa preparation, 8 preferred the benserazide preparation, and 2 had no preference. It is concluded that there is no significant difference in therapeutic effects or adverse reactions between the two commercially available decarboxylase inhibitor-containing preparations. Central-nervous-system actions and side-effects depend on the daily dose of levodopa, regardless of the different ratios of decarboxylase inhibitors to levodopa.

Aged↗

PubMed1980

TSH and prolactin stimulation by the decarboxylase inhibitor benserazide in primary hypothyroidism.

200 mg of the 4-aromatic amino acid decarboxylase inhibitor benserazide were administered orally to five patients with primary hypothyroidism. Benserazide induced a significant increase in prolactin and TSH plasma concentration in all subjects. Since the drug blocks the conversion of DOPA to dopamine, these hormonal changes may be due to a reduction in circulating and/or median eminence levels of dopamine.

Adult↗

PubMed1979

Lack of counteracting effect of liposomes on benserazide-induced hyperprolactinemia.

Benserazide induces an increase of serum prolactin in man, possibly as the result of an impairment of the dopamine effect on the pituitary and/or on the outer median eminence caused by the inhibition on L-dopa decarboxylase. On the other hand, liposomes obtained from bovine brain cortex phospholipids reduced serum prolactin possibly through an effect of phosphatidylserine on dopamine biosynthesis at the level of tyrosine hydroxylase. Benserazide, given orally (125 mg) to 5 normal subjects, induced an increase of serum prolactin that did not change when 300 mg of phospholipid liposomes were given intravenously 60 min later. An increase of L-dopa synthesis does not seen to be capable to overcome the effects of the decarboxylase inhibition.

Adult↗