Antioxidants prevent the interaction of 3,4-dihydroxyphenylacetic acid at the dopamine D2 receptor.
Antioxidants such as ascorbic acid (AA) and dithiothreitol (DTT), can prevent 3,4-dihydroxyphenylacetic acid (DOPAC) inhibition of [3H]spiperone binding to neuronal dopamine D2 receptors. The DOPAC quinone produced from auto-oxidation is believed to be responsible for the irreversible inhibition noted. Quinone conjugation to proteins occurs readily in vivo, and thus, auto-oxidation of DOPAC and other endogenous catechol containing compounds could be an important component of protein modification during on-going neuronal physiology.
Cammack
J
J
Department of Pharmacology and Toxicology, University of Kansas, Lawrence 66045.
Tessel
R
R
Michaelis
E
E
Adams
R N
RN
D015102:3,4-Dihydroxyphenylacetic Acid / Q000378:metabolism / Q000494:pharmacology*; D001205:Ascorbic Acid / Q000494:pharmacology*; D001665:Binding Sites; D003342:Corpus Striatum / Q000187:drug effects / Q000378:metabolism; D004229:Dithiothreitol / Q000494:pharmacology*; D066298:In Vitro Techniques; D009474:Neurons / Q000187:drug effects* / Q000378:metabolism; D010084:Oxidation-Reduction; D011954:Receptors, Dopamine / Q000378:metabolism*; D017448:Receptors, Dopamine D2; D013134:Spiperone / Q000378:metabolism*
D011954:Receptors, Dopamine; D017448:Receptors, Dopamine D2; D015102:3,4-Dihydroxyphenylacetic Acid; D013134:Spiperone; D001205:Ascorbic Acid; D004229:Dithiothreitol