L-Dopa is Found in These Foods
L-Dopa Health Effects
- Anti encephalopathic
- Anti feedant
- Anti morphinic
- Anti neuroleptic
- Anti reserpine
- Anti tremor
- Central nervous system active
- Metabolism: 95% of an administered oral dose of levodopa is pre-systemically decarboxylated to dopamine by the L-aromatic amino acid decarboxylase (AAAD) enzyme in the stomach, lumen of the intestine, kidney, and liver. Levodopa also may be methoxylated by the hepatic catechol-O-methyltransferase (COMT) enzyme system to 3-O-methyldopa (3-OMD), which cannot be converted to central dopamine. Half Life: 50 to 90 minutes
- Uses/Sources: For the treatment of idiopathic Parkinson's disease (Paralysis Agitans), postencephalitic parkinsonism, symptomatic parkinsonism which may follow injury to the nervous system by carbon monoxide intoxication, and manganese intoxication.
- Treatment: Hospitalization is advised, and general supportive measures should be employed, along with immediate gastric lavage and repeated doses of charcoal over time. This may hasten the elimination of entacapone in particular, by decreasing its absorption/reabsorption from the GI tract. Intravenous fluids should be administered judiciously and an adequate airway maintained. The adequacy of the respiratory, circulatory and renal systems should be carefully monitored and appropriate supportive measures employed. Electrocardiographic monitoring should be instituted and the patient carefully observed for the development of arrhythmias; if required, appropriate antiarrhythmic therapy should be given. The possibility that the patient may have taken other drugs, increasing the risk of drug interactions (especially catechol-structured drugs) should be taken into consideration. Hemodialysis or hemoperfusion is unlikely to reduce entacapone levels due to its high binding to plasma proteins. (L1712)
- Route of Exposure: Levodopa is rapidly absorbed from the proximal small intestine by the large neutral amino acid (LNAA) transport carrier system.
- Carcinogenicity: No indication of carcinogenicity to humans (not listed by IARC).
- Toxicity: LD50: 2363 mg/kg (Oral, Mouse) (A308) LD50: 609 mg/kg (Oral, Rabbit) (A308) LD50: 1780 mg/kg (Oral, Rat) (A308)
Mechanism of Action
|Target Name||Mechanism of Action||References|
Solute carrier family 15 member 1
D(4) dopamine receptor
D(3) dopamine receptor
D(1B) dopamine receptor
D(2) dopamine receptor
D(1A) dopamine receptor
|Striatal dopamine levels in symptomatic Parkinson's disease are decreased by 60 to 80%, striatal dopaminergic neurotransmission may be enhanced by exogenous supplementation of dopamine through administration of dopamine's precursor, levodopa. A small percentage of each levodopa dose crosses the blood-brain barrier and is decarboxylated to dopamine. This newly formed dopamine then is available to stimulate dopaminergic receptors, thus compensating for the depleted supply of endogenous dopamine.||