Betreff: Autism/em bits |
Von: Mobile phone mast network |
Datum: Sat, 27 May 2006 00:21:45 +0100 |
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http://epubl.luth.se/1402-1528/1999/20/
Research report / 1999:20
Deficient Synthesis of Nitric Oxide - a Candidate for
an Etiology for Autism
FöRFATTARE: Gustafsson, Lennart
DATUM: 1999-11-01
INSTITUTION: Systemteknik / Industriell elektronik
Abstract
It is commonly accepted that the autistic syndromes are
caused by neurological dysfunctions. Hermelin's observations of
information processing dysfunctions in autism and Frith's theory of a
lack of drive for central coherence delineate essential cognitive
characteristics in autism. Inadequate cortical feature maps has been
proposed as a neural-level theory of autism. The consequences of this
theory are in agreement with Hermelin's observations and Frith's
theory. In this paper it is argued that deficient synthesis of nitric
oxide will cause inadequate cortical feature maps and also will result
in impaired learning in cerebellum and hippocampus. Deficient synthesis
of nitric oxide will also cause some specific characteristics, observed
in autism. It is proposed that deficient synthesis from neuronal Nitric
Oxide Synthase is most likely involved.
ISSN 1402-1528 / ISRN LTU-FR--99/20--SE / NR 1999:20
Clin Chim Acta. 2003 May;331(1-2):111-7.
Changes in nitric oxide levels and antioxidant enzyme
activities may have a role in the pathophysiological mechanisms
involved in autism.
Sogut S, Zoroglu SS, Ozyurt H, Yilmaz HR, Ozugurlu F, Sivasli E, Yetkin O, Yanik M, Tutkun H, Savas HA, Tarakcioglu M, Akyol O.
Department of Biochemistry, Faculty of Medicine,
BACKGROUND: There is evidence that oxygen free radicals play an important role in the pathophysiology of many neuropsychiatric disorders. Although it has not been investigated yet, several recent studies proposed that nitric oxide (NO) and other parameters related to oxidative stress may have a pathophysiological role in autism. METHODS: We assessed the changes in superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) activities and thiobarbituric acid-reactive substances (TBARS) levels in plasma as well as NO levels in red blood cells (RBC) in patients with autism (n=27) compared to age- and sex-matched normal controls (n=30). RESULTS: In the autistic group, increased RBC NO levels (p<0.0001) and plasma GSH-Px activity (p<0.0001) and unchanged plasma TBARS levels and SOD activity were detected. CONCLUSIONS: These findings indicate a possible role of increased oxidative stress and altered enzymatic antioxidants, both of which may be relevant to the pathophysiology of autism.
Cell Biochem Funct. 2003 Mar;21(1):55-60
Pathophysiological role of nitric oxide and
adrenomedullin in autism.
Zoroglu SS, Yurekli M, Meram I, Sogut S, Tutkun H, Yetkin O, Sivasli E, Savas HA, Yanik M, Herken H, Akyol O.
Department of Child and Adolescent Psychiatry,
Several studies indicate that nitric oxide (NO) is involved in the aetiopathogenesis of many neuropsychiatric disorders such as schizophrenia, bipolar disorder, depression, Alzheimer's disease, Hungtington disease and stroke. Although it has not been investigated yet, several recent studies proposed that NO may have a pathophysiological role in autism. Adrenomedullin (AM), a recently discovered 52-amino acid peptide hormone, induces vasorelaxation by activating adenylate cyclase and also by stimulating NO release. AM immune reactivity is present in the brain consistent with a role as a neurotransmitter. It has been stated that NO and AM do function in the regulation of many neurodevelopmental processes. We hypothesized that NO and AM activities have been affected in autistic patients and aimed to examine these molecules. Twenty-six autistic patients and 22 healthy control subjects were included in this study. AM and total nitrite (a metabolite of NO) levels have been measured in plasma. The mean values of plasma total nitrite and AM levels in the autistic group were significantly higher than control values, respectively (p < 0.001, p = 0.028). There is no correlation between total nitrite and AM levels (r = 0.11, p = 0.31). Certainly, this subject needs much further research investigating autistic patients in earlier periods of life and with subtypes of the disorder.
http://www.febs-iubmb-2005.com/abs_abs.php?aid=590
H2 Oxidation of Proteins
Oral: July 4 2005 15:30-18:30, Room 2a and optionally Room 2b
Poster: July 4 13:30-15:30, Building-A, Section-5
H2-017P - Poster presentation
L-Glutamine effect on liver citrulline level
J. I. Nikolic1, D. T. Sokolovic1 and B. J. Djindjic2
1Department of Biochemistry,
Trauma, systemic inflamation, sepsis or toxins can modulate tissue functions. Glutamine has been shown to have beneficial effects in sepsis, trauma, infections, chemotherapy etc. The aim of this study was to investigate the possible beneficial effect of L-glutamine on acute hepatotoxicity induced by mercury chloride (HgCl2). To study possible role of nitric oxide in mechanisms toxicity of mercury chloride we have study interaction between L-Glutamine and nitric oxide synthesis in tissue metabolism. Male Spraque Dawley rats weighing about 200 g. were used in the experiment. Acute toxicity was induced by i.p administration of mercury chloride in a dose of 3mg/kg. One group of animals was pretreated with L-glutamine (200 mg/kg) 1 hour before mercury chloride administration. Control group of animals was treated with equal volume of saline. The animals were killed 24 hours after HgCl2 administration. The level of citrulline, by product in nitric oxide synthesis, was measured by diacetylmonoxime reaction. Results of the study show that acute toxicity of mercury chloride leads to elevation of tissue level of citrulline compared to control group (p<0.01). Administration of glutamine to control rats decreases slowly citrulline level compared to control, while pretreatment of animals with Glutamine before mercury chloride administration leads to the most greater decreases in citrulline level (p< 0.01). Bearing in mind that overproduction of nitric oxide has cytotoxic effects administration of L-Glutamine may be beneficial in mercury toxicity through decreasing nitric oxide level.
http://www.pnas.org/cgi/content/abstract/100/16/9566
PNAS | August 5, 2003 | vol. 100 | no. 16 | 9566-9571
Neuroscience
Nitric oxide negatively regulates mammalian adult
neurogenesis
----- Original Message -----From: Mobile phone mast networkSent: Friday, May 26, 2006 8:49 PMSubject: [Masts] autism/em bits
Medical hypothesis -A possible link between mirror neurons, autism and electromagnetic radiationPossible assoc. between autism and foetal/neo-natal exposure to em fields (Kane) - http://omega.twoday.net/stories/224062/Firstenberg & Molloy on ES - autism incidence - http://www.mindfully.org/Health/2002/Electrical-Sensitivity-Firstenberg1jul02.htmfrom Catherine (via artjar)