Biochemical properties and kinetic parameters of dihydroxyphenyialanine – 5-hydroxytryptophan decarboxylase in brain, liver, and adrenals of cat

1979 ◽  
Vol 57 (7) ◽  
pp. 1014-1018 ◽  
Author(s):  
Sylvie Bouchard ◽  
Andrée G. Roberge

Biochemical properties and kinetic parameters of nonpurified dihydroxyphenylaianine –5-hydroxytryptophan decarboxylase extracted from brain and two peripheral organs, liver and adrenals, were studied in the cat. This study shows that decarboxylase activity in brain is lower than in peripheral organs and that 5-hydroxytryptophan can be decarboxylated without exogenous addition of pyridoxal-5′-phosphate (PLP). However, the addition of PLP substantially increases the enzyme activity. Excess of coenzyme (>60 μM) induces inhibition in adrenals and liver but not in the central nervous system (CNS). The observed inhibition might be related to the presence of a tetrahydroisoquinoline derivative formed in the medium. Differentiation between mechanisms of action of decarboxylase in the CNS and peripheral organs is suggested.

2018 ◽  
Vol 6 (6) ◽  
pp. e00447 ◽  
Author(s):  
Agnès Poirier ◽  
Marla Weetall ◽  
Katja Heinig ◽  
Franz Bucheli ◽  
Kerstin Schoenlein ◽  
...  

1968 ◽  
Vol 108 (2) ◽  
pp. 207-209 ◽  
Author(s):  
G B Ansell ◽  
Sheila Spanner

1. The plasmalogenase activity of brain was found to be associated with the white matter but was absent from myelin fractions. 2. Increased enzyme activity was found in demyelinating spinal cords from vitamin B12-deficient monkeys and in white matter from a patient with multiple sclerosis.


2010 ◽  
Vol 2010 ◽  
pp. 1-16 ◽  
Author(s):  
Sílvia Sisó ◽  
Lorenzo González ◽  
Martin Jeffrey

Prion disorders are infectious, neurodegenerative diseases that affect humans and animals. Susceptibility to some prion diseases such as kuru or the new variant of Creutzfeldt-Jakob disease in humans and scrapie in sheep and goats is influenced by polymorphisms of the coding region of the prion protein gene, while other prion disorders such as fatal familial insomnia, familial Creutzfeldt-Jakob disease, or Gerstmann-Straussler-Scheinker disease in humans have an underlying inherited genetic basis. Several prion strains have been demonstrated experimentally in rodents and sheep. The progression and pathogenesis of disease is influenced by both genetic differences in the prion protein and prion strain. Some prion diseases only affect the central nervous system whereas others involve the peripheral organs prior to neuroinvasion. Many experiments undertaken in different species and using different prion strains have postulated common pathways of neuroinvasion. It is suggested that prions access the autonomic nerves innervating peripheral organs and tissues to finally reach the central nervous system. We review here published data supporting this view and additional data suggesting that neuroinvasion may concurrently or independently involve the blood vascular system.


1996 ◽  
Vol 28 (4) ◽  
pp. 417-424 ◽  
Author(s):  
MARIA ENRICA FERRETTI ◽  
DARIO SONETTI ◽  
MARIA CRISTINA PARESCHI ◽  
MARCO BUZZI ◽  
MARIA LUISA COLAMUSSI ◽  
...  

2019 ◽  
Vol 2019 ◽  
pp. 1-19 ◽  
Author(s):  
Chaoran Chen ◽  
Xiang Zhou ◽  
Jialiang He ◽  
Zhenxing Xie ◽  
Shufang Xia ◽  
...  

Ischemia-reperfusion (I/R) injury is a common pathological process, which may lead to dysfunctions and failures of multiple organs. A flawless medical way of endogenous therapeutic target can illuminate accurate clinical applications. γ-Aminobutyric acid (GABA) has been known as a marker in I/R injury of the central nervous system (mainly in the brain) for a long time, and it may play a vital role in the occurrence of I/R injury. It has been observed that throughout cerebral I/R, levels, syntheses, releases, metabolisms, receptors, and transmissions of GABA undergo complex pathological variations. Scientists have investigated the GABAergic enhancers for attenuating cerebral I/R injury; however, discussions on existing problems and mechanisms of available drugs were seldom carried out so far. Therefore, this review would summarize the process of pathological variations in the GABA system under cerebral I/R injury and will cover corresponding probable issues and mechanisms in using GABA-related drugs to illuminate the concern about clinical illness for accurately preventing cerebral I/R injury. In addition, the study will summarize the increasing GABA signals that can prevent I/R injuries occurring in peripheral organs, and the roles of GABA were also discussed correspondingly.


2009 ◽  
Vol 1;12 (1;1) ◽  
pp. 269-280
Author(s):  
Howard Smith

Despite nearing the end of the decade of pain research, the analgesic mechanisms of one of the most widely used and popular analgesics remains uncertain. Acetaminophen (APAP) (paracetamol [PARA]) has been used clinically for over a half of a century and although clinicians seem to be comfortable with its benefits, risks, and limitations, they still remain in the dark as to precisely what is providing its pain relief. What does seem clearer is that the predominant mechanisms of APAP’s analgesic effects are in the central nervous system (CNS). Although, which central effects are largely responsible for APAP’s effects on pain continue to be uncertain. Perhaps, the most accepted theory is that of APAP’s positive effects on the serotonergic descending inhibitory pathways. However, interactions with opioidergic systems, eicosanoid systems, and/or nitric oxide containing pathways may be involved as well. Furthermore, endocannabinoid signaling may play a role in APAP’s activation of the serotonergic descending inhibitory pathways. A greater understanding of APAP’s analgesic mechanisms may promote optimal utilization of analgesic polypharmacy. Key words: Acetaminophen (APAP), paracetamol (PARA), pain, analgesia, mechanisms of action, serotonin, opioids, endocannabinoids


Toxicon ◽  
1978 ◽  
Vol 16 (3) ◽  
pp. 245-251 ◽  
Author(s):  
Nisson Schechter ◽  
Indhira C. Handy ◽  
Leo Pezzementi ◽  
Jakob Schmidt

1995 ◽  
Vol 2 (1) ◽  
pp. 25-28 ◽  
Author(s):  
Kazuma Fujimoto ◽  
Hidesuke Morita ◽  
Chika Matsunaga ◽  
Shin-ichi Ogata ◽  
Noriaki Furukawa ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document