Pharmacological modification of the serotonergic transmitter system and β-N-acetylhexosaminidase activity in rats

Casal, J.; Corzo, Marı́a D.; Pérez, Luis Francisco; Alvarez, Jean‐Claude; Aldegunde, M.; Tutor, J. Carlos

doi:10.1016/s0024-3205(00)00817-1

Cited by 2 publications

(2 citation statements)

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“…The behavioral and physiological features of this syndrome include hypolocomotion, head twitch, forepaw treading, tremors, hindlimb abduction, flat body posture or hunched back, cyanosis, and hyperthermia. In rodents, 5-HTP induces a serotonin syndrome at dosages of 100-200 mg/ kg (Casal et al, 2000;Nisijima et al, 2000Nisijima et al, , 2001; see Section 4.4.3 for more on serotonin syndrome). This 5-HTP-induced syndrome is potentiated by SSRIs.…”

Section: Factors Affecting 5-hydroxytryptophan Availability For Serotmentioning

confidence: 99%

Serotonin a la carte: Supplementation with the serotonin precursor 5-hydroxytryptophan

Turner

Loftis

Blackwell

2006

Pharmacology & Therapeutics

270

158

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This paper reviews the preclinical and clinical evidence regarding the use of the dietary supplement 5-hydroxytryptophan (5-HTP) for the treatment of depression. In the absence of supplementation with exogenous 5-HTP, the amount of endogenous 5-HTP available for serotonin synthesis depends on the availability of tryptophan and on the activity of various enzymes, especially tryptophan hydroxylase, indoleamine 2,3-dioxygenase, and tryptophan 2,3-dioxygenase (TDO). Factors affecting each of these are reviewed. The amount of 5-HTP reaching the central nervous system (CNS) is affected by the extent to which 5-HTP is converted to serotonin in the periphery. This conversion is controlled by the enzyme amino acid decarboxylase, which, in the periphery, can be blocked by peripheral decarboxylase inhibitors (PDIs) such as carbidopa. Preclinical and clinical evidence for the efficacy of 5-HTP for depression is reviewed, with emphasis on double-blind, placebo-controlled (DB-PC) trials. Safety issues with 5-HTP are also reviewed, with emphasis on eosinophilia myalgia syndrome (EMS) and serotonin syndrome. D

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Section: Factors Affecting 5-hydroxytryptophan Availability For Serotmentioning

confidence: 99%

Serotonin a la carte: Supplementation with the serotonin precursor 5-hydroxytryptophan

Turner

Loftis

Blackwell

2006

Pharmacology & Therapeutics

270

158

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“…For some years we have been working on the possible thermodynamic characterization of the enzyme heterogeneity of Hex in different physiopathological situations (21,(23)(24)(25)(26)(27)(28)(29)(30)(31)(32). The enzyme activities are determined at 25º, 30º, 35º and 37ºC with a Cobas Bio analyzer (Roche Diagnostics) using the neutral chromogenic substrate 3,3'-dichlorophenolsulfonphthaleinyl N-acetyl-ß-D-glucosaminide, and the Arrhenius plots and the apparent activation energies are calculated.…”

Section: Biochemical Characterization Of Homozygous and Heterozygous mentioning

confidence: 99%

Biochemical characterization of the GM2 gangliosidosis B1 variant

Tutor

2004

Braz J Med Biol Res

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The deficiency of the A isoenzyme of ß-hexosaminidase (Hex) produced by different mutations of the gene that codes for the α subunit (Tay-Sachs disease) has two variants with enzymological differences: the B variant consists of the absence of Hex A isoenzyme and the B1 variant produces an inactive Hex A isoenzyme for the hydrolysis of the GM2 ganglioside and synthetic substrates with negative charge. In contrast to the early childhood form of the B variant, the B1 variant appears at a later clinical stage (3 to 7 years of age) with neurodegenerative symptoms leading to the death of the patient in the second decade of life. The most frequent mutation responsible for the GM2 gangliosidosis B1 variant is R178H, which has a widespread geographic and ethnic distribution. The highest incidence has been described in Portugal, which has been suggested as the point of origin of this mutation. Biochemical characterization of this lysosomal disease is carried out using negatively charged synthetic α subunit-specific sulfated substrates, since Hex A isoenzyme heat-inactivation assays are not applicable. However, the determination of the apparent activation energy of Hex using the neutral substrate 3,3'-dichlorophenolsulfonphthaleinyl N-acetyl-ß-D-glucosaminide, may offer a valid alternative. The presence of an α subunit in the αß heterodimer Hex A means that its activation energy (41.8 kJ/mol) is significantly lower than that of the ßß homodimer Hex B (75.1 kJ/mol); however, as mutation inactivates the α subunit, the Hex A of the B1 variant presents an activation energy that is similar to that of the Hex B isoenzyme. Correspondence

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Pharmacological modification of the serotonergic transmitter system and β-N-acetylhexosaminidase activity in rats

Cited by 2 publications

References 0 publications

Serotonin a la carte: Supplementation with the serotonin precursor 5-hydroxytryptophan

Serotonin a la carte: Supplementation with the serotonin precursor 5-hydroxytryptophan

Biochemical characterization of the GM2 gangliosidosis B1 variant

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