Catecholamines chemistry

The next two examples illustrate more complex surface reaction chemistry that brings about the covalent immobilization of bioactive species such as enzymes and catecholamines. Poly [bis (phenoxy)-phosphazene] (compound 1 ) can be used to coat particles of porous alumina with a high-surface-area film of the polymer (23). A scanning electron micrograph of the surface of a coated particle is shown in Fig. 3. The polymer surface is then nitrated and the arylnitro groups reduced to arylamino units. These then provided reactive sites for the immobilization of enzymes, as shown in Scheme III. 

The final example involves the immobilization of catecholamines, such as dopamine, to a polyphosphazene surface (24). The chemistry is shown in Scheme IV. In this case, conversion of surface... 

Starkey, J. A., Mechref, Y, Muzikar, J., McBride, W. J., and Novotny, M. V., Determination of salsolinol and related catecholamines through on-line preconcentration and liquid chromatography/atmospheric pressure photoionization mass spectrometry. Analytical Chemistry 78(10), 3342-3347, 2006. 

Assay procedures for dopamine which are superficially similar to the lutin procedure described above have been reported recently.266-268 The chemistry of the production of the fluorophore from dopamine is, however, somewhat different since the fluorophore is not a 5,6-dihydroxyindoxyl, it is incorrect to refer to the trihy-droxyindole fluorophore of dopamine (cf. ref. 252). Oxidation of the extracted catecholamine is usually carried out with iodine,266-268 presumably with the formation of 7-iodonorepinochrome. The aminochrome is subsequently rearranged to 5,6-dihydroxyindole (it is probable that deiodination accompanies the rearrangement in this case) by a solution of sodium sulfite in aqueous alkali the solution is acidified before measuring the fluorescence of the product (which is said to form relatively slowly and to be very stable).266-268 Irradiation of the reaction mixture with ultraviolet light accelerates the maximal development of fluorescence.266 Since acidification will produce sodium bisulfite in the reaction mixture, it is probable that the fluorophore is a 5,6-dihydroxyindole-sodium bisulfite addition complex. Complexes of this type are known to be both fluorescent and relatively stable in dilute acid solution.118 123,156 265 They also form relatively slowly.255... 

Another theory of mental illness postulates endogenous alkaloid formation. Aldehydes formed by oxidation of catecholamines as well as formaldehyde and acetaldehyde are present in tissues in small amounts. Condensation with amines could generate Schiff bases and alkaloids as in Fig. 25-10. This "plant chemistry" is spontaneous and can apparently take place in the brain, where it may have a potent effect. 

Cocaine [50-36-2] - [ALKALOIDS] (Vol 1) - [ALKALOIDS] (Vol 1) -and catecholamines [EPINEPHRINE AND NOREPINEPHRINE] (Vol 9) -forensic testing for [FORENSIC CHEMISTRY] (Vol 11) -substance abuse of [PSYCHOPHARMACOLOGICAL AGENTS] (Vol 20)... 

Drugs can cause false results in clinical chemistry tests, e.g. plasma cortisol, urinary catecholamine, urinary glucose. 

Derivatization is important in capillary electrophoresis to enhance the detectibility of solutes that are nonfluorescent [7]. The chemistry can occur precapillary, on capillary, postcapillary. Typically, the solutes are amino acids, catecholamines, peptides, or proteins, all of which contain primary or secondary amine groups. 

Lee, N.S., Hsieh, Y.Z., Paisley, R.F., and Morris, M.D. (1988) Surface-enhanced Raman spectroscopy of the catecholamine neurotransmitters and related compoimds. Analytical Chemistry, 60, 112 446. 

CioUcowski, E.L., Maness, K.M., Cahill, P.S., Wightman, R.M., Evans, D.H., Eosset, B., and Amatore, C. 1994. Disproportionation during electrooxidation of catecholamines at carbon-fiber microelectrodes. Analytical Chemistry 66, 3611-3617. 

The naturally occurring catecholamines dopamine (1), norepinephrine (2), and epinephrine(3) (Figure 1) play key roles in neurotransmission, metabolism, and in the control of various physiological processes. For example, norepinephrine is the primary neurotransmitter in the sympathetic nervous system and also functions as a neurotransmitter in the central nervous system. Epinephrine, elaborated by the adrenal gland, has potent effects on the heart, vascular and other smooth muscles. Dopamine is an important neurotransmitter in the central nervous system, and has important peripheral effects in such organs as the kidney and heart. The importance of these effects has made the search for drugs that can mimic, inhibit, or otherwise modulate the effects of these catecholamines an important area of medicinal chemistry. 

In the past few years, the chemistry and pharmacology of the catecholamines and their metabolic inhibitors have been the subject of intensive investigation in many parts of the world but especially by Sjoerdsma and Axelrod at the National Heart Institute. Monoamine oxidase inhibitors have been tried in the treatment of hypertension with both uncertain results and uncertain rationale. Recently, the decarboxylase inhibitor, methyldopa, has been widely recommended in the treatment of hypertension, though, again, the evidence gives no clear idea as to how it works. 

The early pioneering work by Zeller et al. (115) on the potent MAO inhibitory effect of iproniazid—a structural modification of the tuberculostat Isoniazid—and his realization of the physiologic consequences that might arise from such a profound alteration in catecholamine metabolism, the actual confirmation by Brodie, Pletscher, and Shore (27) of the rise in brain monoamine levels following the administration of iproniazid and JB-516 (a-methylphen-ethylhydrazine), and the early euphoric effects noted by Selikoff, Robitzek, and Omstein (96) in tuberculosis patients on iproniazid therapy led Kline and his associates (67) to investigate the possible application of iproniazid in the treatment of mental depression. It was their conclusion that MAO inhibition and antidepressant effect had a causal relationship and that a new approach for the treatment of mental depression had been uncovered. The subject of the MAO inhibitors has been reviewed extensively up to 1960 by Pletscher, Gey, and Zeller (84) and by Biel, Horita, and Drukker (21) to 1963, in comprehensive reviews of the chemistry, biochemistry, pharmacology, clinical application, and structure-activity relationships of the MAO inhibitors. 

K.T. Kawagoe, J.A. Jankowski and R.M. Wightman, Etched carbon-fiber electrodes as amperometric detectors of catecholamine secretion from isolated biological cells. Analytical Chemistry, 63(15), 1589-1594 (1991). 

P. Chen, B. Xu, N. Tokranova, X.J. Feng, J. Castracane and K.D. Gillis, Amperometric detection of quantal catecholamine secretion from individual cells on micromachined silicon chips, Analytical Chemistry, 75(3), 518-524 (2003). 

Adrenergic Systems. Over the past few years, significant advances in our understanding of the in-situ chemistry of both the a- and -receptors for catecholamines have been made. We shall examine briefly some... 

In Chapter 8, peripheral aspects of the cholinergic system were considered. The basics of the neuron (Fig. 8-1), specifically the cholinergic neuron (Fig. 8-5), the synapse (Fig. 8-2), and depolarization (Fig. 8-3), were also presented. The significance and chemistry of acetylcholine (ACh) was discussed. Chapter 9 continued with the remainder of the peripheral autonomic nerve plan (i.e., the sympathetic, or adrenergic, system). The biosynthesis of the catecholamines DA, NE, and EP were discussed and illustrated (Fig. 9-1), and the metabolism schemes for NE and EP (Fig. 9-3) and DA (Fig. 9-4) were outlined. Much of the early (before 1960) neurochemistry elucidated, and neurotransmitters identified, were central to the functioning of the peripheral nervous system. 

---