Tryptophan enhancement

Zhang, R.-G., et al. The crystal structure of trp aporepressor at 1.8 A shows how binding tryptophan enhances DNA affinity. Nature 327 591-S97, 1987. 

Aviram, M., Cogan, U., and Mokady, S., Excessive dietary tryptophan enhances plasma lipid peroxidation in rats, 88, 29, 1991. 

Suzuki S, Tourkina E, Ludwicka A, Hampton M, Bolster M, Maize J, Silver RM (1996) A contaminant of L-tryptophan enhances expression of dermal collagen in a murine model of eosinophilia myalgia syndrome. Proc Assoc Am Physicians, 104 315-322. 

L-tryptophan enhanced the yield of tryptamine, whereas the yield of serpentine was not affected. 

Under the experiment conditions, the enzymatic cleavage occurs within seconds. Therefore, the observed release time of the tryptophan is also the actual disappearance time of the intermediate forms after the enzymatic cleavage. This dramatic enhancement of tail-unit release with the elimination-based system (dendritic molecule 19) compared to the cyclization-based system (dendritic molecule 18) is best viewed by superimposition of the graphs (Fig. 5.13). 

El-Agamey, A., M. Burke, R. Edge et al. 2005. Photolysis of carotenoids in chloroform Enhanced yields of carotenoid radical cations in the presence of a tryptophan ester. Rad. Phys. Chem. 72 341-345. 

The synthesis of 5-HT can increase markedly under conditions requiring more neurotransmitter. Plasticity is an important concept in neurobiology. In general, this refers to the ability of neuronal systems to conform to either short- or long-term demands placed upon their activity or function (see Plasticity in Ch. 53). One of the processes contributing to neuronal plasticity is the ability to increase the rate of neurotransmitter synthesis and release in response to increased neuronal activity. Serotonergic neurons have this capability the synthesis of 5-HT from tryptophan is increased in a frequency-dependent manner in response to electrical stimulation of serotonergic soma [7]. The increase in synthesis results from the enhanced conversion of tryptophan to 5-HTP and is dependent on extracellular calcium ion. It is likely that the increased 5-HT synthesis results in part from alterations in the kinetic properties of tryptophan hydroxylase, perhaps due to calcium-dependent phosphorylation of the enzyme by calmodulin-dependent protein kinase II or cAMP-dependent protein kinase (PKA see Ch. 23). 

The acute and chronic effects of Li+ in patients are quite different (reviewed by Goodnick [146]). Initially, Li+ treatment causes an increase in the level of 5-HT and decrease in 5-HT uptake in platelets, with an increase in the level of 5-HIAA in the CSF. The neuroendocrine responses to the 5-HT precursors, tryptophan and 5-hydroxytryptophan [160], and to flenfluramine [161], a 5-HT releaser, are enhanced by Li+. Thus the combined effect of acute Li+ treatment is to increase the efficiency of synaptic 5-HT. However, chronic Li+administration results in almost the opposite effect, resulting in responses close to the levels... 

A second, more extensive experiment involved oral administration of three daily doses (100 mg/kg) of parachlorophenylalanine (PCPA). This tryptophan hydroxylase inhibitor (47), like reserpine, enhanced the behavioral effects of LSD (13) moreover, hypersensitivity occurred when 5-HT, but not other monoamine, concentrations were below normal in both forebrain and hindbrain (13). That is, effects were observed at 5 and 12 days (when 5-HT was depleted to 10-20% and 60-70% of normal) but not at 21 days (when 5-HT had returned to normal). Control experiments (13) indicated that (a) the interaction of PCPA, 5-HT, and LSD was probably not caused by generalized hyperactivity or hyperirritability sometimes seen after PCPA (73) (b) PCPA does not affect threshold doses of other psychoactive but nonserotonergic compounds, such as d-amphetamine (0.3 mg/kg) and (c) pretreatment with a-methylparatyrosine, a tyrosine hydroxylase inhibitor which depletes catecholamines rather than indoleamines, does not alter sensitivity to LSD. 

Compared to absorbance detection, direct detection of proteins rich in aromatic amino acids by the intrinsic fluorescence of tryptophan and tyrosine residues provides enhanced sensitivity without the complexity of pre- or postcolumn derivatization. The optimal excitation wavelengths for these amino acids are in the 270- to 280-nm range. 

Figure 13.28 A possible mechanism by which increased levels of tryptophan and/or tyrosine can occur in neurones and lead to fatigue. The mechanism proposes that physical activity increases the entry of tryptophan or tyrosine into the neurones which increases the concentration of the neurotransmitters, 5-hydroxy-tryptamine or dopamine, respectively. The neurotransmitters are present in vesicles in the presynaptic terminal (Chapter 14). (The pathways for the formation of 5-hydroxytryptamine and dopamine are described in Chapter 14.) This enhances the amount release into the synapses which decreases the excitation of 5-hydroxytryptamine or dopamine neurones in the motor control pathway. It is assumed that they are inhibitory neurotransmitters, they will reduce electrical activity in the motor control pathway and hence nervous stimulation of muscle fibres. This results in fatigue. Mechanisms by which physical activity might result in increased entry of these amino acids into the brain are presented in Appendix 13.5.

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