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In accordance with Wikipedia:WikiProject_Drugs naming policy, I propose we move this page to the INN levodopa. If you have any concern with this proposal, please discuss it on this page. Matt 18:09, 23 Dec 2004 (UTC)
Under the Therapeutic Use section, I'm pretty sure that this statement is wrong:
"so it is administered with a peripheral DDC (dopamine decarboxylase) inhibitor such as carbidopa"
I believe that it should be "DOPA decarboxylase" instead of "dopamine decarboxylase"
Could you please address this minor fault.
Could someone please include some information on l-dopa in foods? The fava bean, for example, contains a high level of "natural" l-dopa.
The only foods I've heard of containing L-dopa is Fava beans and Mucuna pruriens (also a type of bean in which you can buy in supplement form). — Preceding unsigned comment added by 22.214.171.124 (talk) 14:14, 20 September 2011 (UTC)
Maybe I'm missing something, but wouldn't L-DOPA, being converted in the periphery to dopamine, therefore cause an increase in blood pressure?-Anodyne 25 September 2006
yes yes please answer this question...i thought dopamine would increase blood pressure...and also even after it gets converted to noradrenaline and adrenaline it would still cause hypertension.... i was just wondering if this is the answer...if theres too much adrenaline in blood it causes the fight flight fright responses...then it would direct the blood to the muscles of the legs so it would help us to run faster (to get out of there)and causes other things like increase heart rate and ilke dilation of pupils (to see better) and etc.... so in an overdose of L-dopa you get too much vasodilation in the muscles and too much vessel constriction in the gut and stuff...and the blood pools away in the muscle causing hypotension inside the organs?
As is the premise of the latest episode of House. Why is there no mention of this? It's use of reviving coma victims originated in south africa, its revival only lasts 4 hours. Very interesting, like temporary revival of the dead, just to ask some questions.
House = Fiction. QED. Zerocannon 16:28, 16 October 2007 (UTC)
This not "exactly" fiction, for certain values of exactly.
Here is a more "pop-sci" article if you do not enjoy medical journels
Levodopa increases all of the catecholamines, but mostly dopamine. Since dopamine is an adrenergic, you might exect it to cause hypertension, but it is a selective-beta adrenergic receptor agonist with no significant alpha action. Whereas alpha receptors constrict blood vessels in intestines and stomach and stuff, beta receptors dilate vessels in skeletal muscle to allow more nutrients to go to the muscles. The result is that since levodopa mainly increases dopamine, and dopamine works only on beta receptors, blood vessel only dilate and hypotension can occur. —Preceding unsigned comment added by 126.96.36.199 (talk) 06:45, 14 January 2008 (UTC)
I have added some information on cellular and neuronal toxicity induced by Levodopa in the "Adverse Effects" section of the article, and have provided references to medical research journals for the statements. I believe, however, that such a section should be enlarged to include more of these related issues, as the drug is sold over the counter as a dietary supplement and safety information (especially from extracts) is scarce.
18:03, 8 March 2008 (UTC)
This article should be called L-DOPA. L-DOPA is the common, scientific name for a chemical which exists as a biosynthetic precursor to dopamine and can also be synthesized in the lab. Levadopa is the INN for synthetic L-DOPA intended for use as a pharmaceutical. Since this article is about the substance as a chemical (structure, synthesis, etc.), the natural biological properties (synthesis, function, etc.), and its use as a pharmaceutical (role in Parkinsons, dosing, etc.) we should use the most general name, not the pharmaceutical specific one. --Selket Talk 03:34, 25 July 2008 (UTC)
Large section added by 188.8.131.52 (talk · contribs) that is either original research ("Our observations") or if not personal commentary then is a copy of text from somewhere else which has not been rephrased for encyclopaedic style - failling this, then a conflict of interest to add one's own material directly into articles without discussion in talk page 1st. See WP:No original research and WP:Conflict of interest.
So here is the added text that we might look at:
Several studies show it is not toxic and actually is quite neuroprotective.
Adv Neurol. 2001;86:327-36.L The protective role of levodopa in the human substantia nigra. Rajput AH. Division of Neurology, Royal University Hospital, University of Saskatchewan, Saskatoon, S7N 0W8, Canada.
Laboratory studies and studies of animal models of parkinsonism have produced contradictory evidence, but there is no evidence that LD is toxic to normal substantia nigra in animals. We have studied human subjects longitudinally to address that issue. A cumulative LD dose up to 24 kg was not toxic in one autopsied essential tremor (ET) case. Two other ET patients did not develop parkinsonism on 8.5 kg and 21 kg cumulative LD dose, respectively. One DOPA-responsive dystonia (DRD) case has no evidence of parkinsonism after 29 years and more than 17 kg of LD. A DRD patient who received 3 kg over 11 years had normal SN neuronal complement at autopsy. One patient who has clinical and laboratory evidence of nigral pathology as the basis of parkinsonism when untreated for 18 years had progressive disability. While on LD he has excellent symptomatic benefit and virtual cessation of progression of the disease. Epidemiologic studies indicate that those prescribed LD at an early stage of illness and hence given larger cumulative lifetime doses have longer survival than those in whom LD is started late and who receive smaller total doses. Our observations and the available literature support that levodopa is not toxic to normal or diseased substantia nigra in human beings. Evidence presented here indicates that levodopa has a protective effect on the human substantia nigra neurons.
Mov Disord. 1997 Sep;12(5):634-8.L Is levodopa toxic to human substantia nigra?
Rajput AH, Fenton M, Birdi S, Macaulay R. Division of Neurology, Royal University Hospital, Saskatoon, Saskatchewan, Canada.
Levodopa (LD) is the most effective drug for symptomatic control of Parkinson's disease, but has been suspected to be toxic to substantia nigra (SN) dopaminergic neurons. Tissue culture and animal studies of LD toxicity have produced contradictory evidence, and one study reported that a human subject exposed to a large cumulative dose (cd) of LD over 4 years had no evidence of SN damage. We report the cases of five patients, each of whom received a large cd of LD over a long period. Fluorodopa positron-emission tomography performed in one case indicated parkinsonism. Autopsies in two cases indicated a normal SN in one and a hypopigmented SN with normal cell complement in the other. Three patients had essential tremor, one had nonprogressive parkinsonism, and one had dopa-responsive dystonia. LD (without decarboxylase inhibitor) was administered over 21 years (cd = 21.99 kg), 9 years (cd = 6.6 kg), 26 years (cd = 18.7 kg), 11 years (cd = 3 kg), and 26 years (cd = 23.93 kg), respectively. None of the patients with essential tremor developed clinical features of parkinsonism that indicated significant SN damage, and one had a normal SN at autopsy. The parkinsonian patient displayed no detectable acceleration of disease process, and the patient with dopa-responsive dystonia had a normal complement of SN neurons at autopsy. We conclude that LD, administered at a dose commonly used for treating Parkinson's disease, was not toxic to SN neurons in these cases.
Parkinsonism Relat Disord. 2001 Oct;8(2):95-100. Levodopa prolongs life expectancy and is non-toxic to substantia nigra.
Rajput AH.Neurology Division, Royal University Hospital, 103 Hospital Drive, Saskatoon, SK, Canada S7N 0W8. firstname.lastname@example.org
The primary objective of the study was to determine the effect of levodopa (LD) on human substantia nigra. The study included patients seen at the Movement Disorder Clinic, Saskatoon over a 32 year period. The evidence provided is based on epidemiological observations of 934 consecutive Parkinson syndrome (PS) patients assessed during 22 years and detailed studies of six patients including two autopsies. Life expectancy increased significantly with LD therapy. The prolonged survival was evident when the patients were treated during early stage of the illness. One parkinsonian patient with substantia nigra (SN) pathology who was extensively studied for 30 years, revealed significant slowing of the disease progression while on LD. Three essential tremor patients who received 24 kg (26 years), 22 kg (21.5 years), and 8.5 kg (12.5 years) LD respectively, had no evidence of PS and one autopsy revealed normal SN. Two dopa-responsive dystonia patients who received LD 3 kg (11 years) and 17 kg (29 years) each had no evidence of PS and one autopsy revealed normal number of SN neurons.These observations indicate that LD is not toxic to human SN and are consistent with salutary effect of the drug on the SN in Parkinson's disease.
Mov Disord. 2001 May;16(3):424-34.L Chronic L-DOPA administration is not toxic to the remaining dopaminergic nigrostriatal neurons, but instead may promote their functional recovery, in rats with partial 6-OHDA or FeCl(3) nigrostriatal lesions.
Datla KP, Blunt SB, Dexter DT. Parkinson's Disease Research Unit, Department of Neuroinflammation, Imperial College School of Medicine at Charing Cross Campus, Fulham Palace Road, London W6 8RF, United Kingdom.
In this study, we have examined the effects of chronic L-3,4-dihydroxyphenylalanine (L-DOPA) administration on the remaining dopaminergic neurons in rats with 6-hydroxydopamine (6-OHDA) or buffered FeCl(3) partial lesions to the nigrostriatal tract. L-DOPA administration increased the turnover of dopamine in the striatum. L-DOPA administration for 1 week produced an increase in the level of striatal RTI-121 binding, a specific marker for dopamine uptake sites on the dopaminergic nerve terminals in the striatum. However, longer periods of L-DOPA treatment decreased the level of RTI-121 binding in the striatum. In the partial 6-OHDA lesion model, L-DOPA treatment had a time-dependent effect on the number of neurons demonstrating a dopaminergic phenotype i.e., neurons that are tyrosine hyrdoxylase (TH)-immunopositive, on the lesioned side of the brain. In the first few weeks of treatment, L-DOPA decreased the number of TH-positive neurons but with long-term treatment, i.e., 24 weeks, L-DOPA increased the number of neurons demonstrating a dopaminergic phenotype. Even in the buffered FeCl(3) infusion model, where the levels of iron were increased, L-DOPA treatment did not have any detrimental effects on the number of TH-positive neurons on the lesioned side of the brain. Consequently, chronic L-DOPA treatment does not have any detrimental effects to the remaining dopaminergic neurons in rats with partial lesions to the nigrostriatal tract; indeed in the 6-OHDA lesion model, long-term L-DOPA may increase the number of neurons, demonstrating a dopaminergic phenotype.
J Neurochem. 1996 Feb;66(2):501-10. L-DOPA up-regulates glutathione and protects mesencephalic cultures against oxidative stress.
Irrespective of the value of the studies mentioned, wikipedia does not generally give abstracts of studies, rather it states a fact or opinion and then cites the source, allowing readers to go and look at the details (providing PubMed links will allow linkage online to the abstracts) David Ruben Talk 00:52, 3 September 2008 (UTC)
Jytdog (talk) 23:22, 26 August 2009 (UTC)moved the paragraph on "Epigallocatechin gallate" from Drugs to Dietary Supplements, as Epigallocatechin gallate is not a drug. This is some academic research and we don't want people thinking Epigallocatechin gallate is a drug.
Under side effects it states: "Disturbed respiration, which is not always harmful, and can actually benefit patients with upper airway obstruction"
This is somewhat counter-intuitive and contrary to basic emergency medicine. I would like citation, clarification, or removal. It is possible that this is simply a miscomunication and would benifit from a better explination/clarifiction (Croaker260 (talk) 20:22, 27 February 2012 (UTC))
The following were appended to the references section, but are currently not used to support any specific article content as far as I can tell. I'm moving them here in case anyone would like to use them to expand the article. -- Ed (Edgar181) 13:08, 1 May 2012 (UTC)
So under the side effects section, possible neurotransmitter depletion was placed there, without a citation.
I found a paper in the literature (5-HTP efficacy and contraindications), but the ideas seem sketchy to me. While competitive inhibition is certainly possible, they repeatedly cite themselves, and many of their previous papers appear to be bordering on what is colloquially called "bro-science" - unsubstantiated and often dramatic claims, or poor quality experiments/studies. Could someone else please take a look at this source and verify its credibility? (Erebusthedark (talk) 23:46, 5 March 2014 (UTC))