Disease relevance of DL-threo-3,4-Dihydroxyphenylserine

• DL-Threo-3,4-dihydroxyphenylserine does not exert a pressor effect in orthostatic hypotension [1].
• Orthostatic hypotension in a patient with Shy-Drager syndrome was treated for 6 months with oral DL-threo-3,4-dihydroxyphenylserine (DL-threo-DOPS) [2].
• DL-threo-3,4-dihydroxyphenylserine for freezing symptom in parkinsonism [3].
• After the patient received DL-threo-DOPS, the fall in his mean arterial blood pressure on head-up tilting was reduced and he had no syncope when standing [2].
• Catecholamine metabolism during additional administration of DL-threo-3,4-dihydroxyphenylserine to patients with Parkinson's disease [4].

High impact information on DL-threo-3,4-Dihydroxyphenylserine

• Golden hamsters received intraperitoneal injections of the norepinephrine precursor DL-threo-dihydroxyphenylserine, the dopamine precursor L-3,4-dihydroxyphenylalanine, or the serotonin precursor 5-hydroxytryptophan with and without pretreatment of the hamsters with the monoamine oxidase inhibitor tranylcypromine [5].
• Orthostatic hypotension in familial amyloid polyneuropathy: treatment with DL-threo-3,4-dihydroxyphenylserine [6].
• A group of amnesic patients with Korsakoff's disease were treated with a single 1 g dose of DL-threo-3,4-dihydroxyphenylserine (DOPS) and placebo (lactose) in a double-blind crossover study [7].
• Treatment with the synthetic amino acid, DL-threo-dihydroxyphenylserine, which is converted to noradrenaline by dopa-decarboxylase, resulted in a significant increase in blood pressure [8].
• Thus, both amino acids may be useful as precursors of central NE when its level is depleted (e.g. following administration of DSP-4); DL-threo-DOPS producing a generalized increase in brain NE turnover, while increases following tyrosine are specific to those areas in which neuronal activity is increased i.e. cortex and hippocampus [9].

Chemical compound and disease context of DL-threo-3,4-Dihydroxyphenylserine

• A 77-year-old man with Parkinson's disease of long standing, under treatment with L-DOPA and benserazide, was administered DL-threo-3, 4-dihydroxyphenylserine (DL-threo-DOPS), a precursor of norepinephrine, for 10 days [10].
• DL-threo-3,4-dihydroxyphenylserine (DL-threo-DOPS) was administered during 10 days to 4 patients with longstanding Parkinson's disease in addition to their treatment with L-3,4-dihydroxyphenyl-L-alanine (L-DOPA)-carbidopa (Sinemet) [4].

Biological context of DL-threo-3,4-Dihydroxyphenylserine

• In addition measurements in urine reveals that at the dose used Sinemet prevents peripheral decarboxylation of DL-threo-DOPS into noradrenaline [4].
• One of the following substances: L-beta-3, 4-dihydroxyphenylalanine (L-DOPA), DL-threo-dihydroxyphenylserine (DOPS), or 5-hydroxy-L-tryptophan (5-HTP) was administered intraperitoneally at 0900h on the expected diestrus day 2 (D2) [11].
• Intraperitoneal injection of L-beta-3, 4-dihydroxyphenylalanine (L-DOPA), DL-threo-dihydroxyphenylserine (DOPS), or 5-hydroxy-L-tryptophan (5-HTP) suppressed food intake [12].

Anatomical context of DL-threo-3,4-Dihydroxyphenylserine

• The amino acids tyrosine and DL-threo-3,4-dihydroxyphenylserine (DL-threo-DOPS) were compared for their effectiveness in increasing central nervous system norepinephrine (NE) turnover in both saline and DSP-4 pretreated mice [9].
• During the DL-threo-DOPS-treatment cerebrospinal fluid (CSF), serum and urine concentrations of catecholamines were measured [4].
• These observations suggest that DL-threo-DOPS can pass through the blood-brain barrier and change to norepinephrine, and that DL-threo-DOPS may be beneficial in the treatment of the freezing phenomenon of Parkinson's disease [10].

References