ok, are we just over looking this mold or what?

[Guest guest]

I checked on several know web sites and it's mention as a indoor mold but

basicly a allergen if anything. ARTHRINIUM

and is this the mycotoxins it produces? 3-NITROPROPIONIC ACID

I was just pretty amased when I started reading about this mold

2008 Neurobiology of Disease

Decreased Striatal Dopamine Release Underlies Increased Expression of Long-Term

Synaptic Potentiation at Corticostriatal Synapses 24 h after

3-Nitropropionic-Acid-Induced Chemical Hypoxia

http://www.jneurosci.org/cgi/content/full/28/38/9585

3-NP MYCOTOXIN/BEHAVIORAL ALTERATIONS

http://www.fpgrahamco.com/pdfs/8_3_4_7.pdf

2009 GREEN TEA/3-NP

http://www.merckmedicus.com/pp/us/hcp/hcp_newsarticle.jsp?newsid=1231561 & newsgro\

up=2

3-NP MYCOTOXIN,BRAIN/TOXICITY EFFECTS/ARTHRINIUM CONTAMINATED SUGAR CANE

http://ntp.niehs.nih.gov/index.cfm?objectid=E8803E54-BDB5-82F8-F4F502B9D4AC7980

Cellular/Molecular/2003/CITED

Neurodegeneration in Striatum Induced by the Mitochondrial Toxin

3-Nitropropionic Acid: Role of Matrix Metalloproteinase-9 in Early Blood-Brain

Barrier Disruption?

http://www.jneurosci.org/cgi/content/abstract/23/25/8733

SOD1,BONE MARROW/3-NP

http://people.bu.edu/gaowx/Huang-G93A-NL2007.pdf

NICOTINE TREATMENT/PARKINSON'S AND HUNTINGSTON'S DISEASE

2005 Sep 30;67(1-2):161-8.

Neuroprotective effect of nicotine against 3-nitropropionic acid (3-NP)-induced

experimental Huntington's disease in rats.

Tariq M, Khan HA, Elfaki I, Al Deeb S, Al Moutaery K.

Neuroscience Research Group, Armed Forces Hospital, P.O. Box 7897 (W-912),

Riyadh 11159, Saudi Arabia. rkh_research.

Nicotinic acetylcholine receptors (nAChRs) are regarded as potential therapeutic

targets to control various neurodegenerative diseases. Owing to the relevance of

cholinergic neurotransmission in the pathogenesis of Huntington's disease (HD)

this investigation was aimed to study the effect of nicotine, a nAChR agonist,

on 3-nitropropionic acid (3-NP)-induced neurodegeneration in female Wistar rats.

Systemic administration of 3-NP in rats serves as an important model of HD. The

animals received subcutaneous injections of nicotine (0, 0.25, 0.50 and 1.00

mg/kg) daily for 7 days. 3-NP (25 mg/kg, i.p.) was administered daily 30 min

after nicotine for the same duration. One additional group of rats served as

control (vehicle only). On day 8, the animals were observed for neurobehavioral

performance (motor activity, inclined plane test, grip strength test, paw test

and beam balance). Immediately after behavioral studies, the animals were

transcardially perfused with neutral buffered formalin (10%) and brains were

fixed for histological studies. Lesions in the striatal dopaminergic neurons

were assessed by immunohistochemical method using tyrosine hydroxylase (TH)

immunostaining. Treatment of rats with nicotine significantly and

dose-dependently attenuated 3-NP-induced behavioral deficits. Administration of

3-NP alone caused significant depletion of striatal dopamine (DA) and

glutathione (GSH), which was significantly and dose-dependently attenuated by

nicotine. Preservation of striatal dopaminergic neurons by nicotine was also

confirmed by immunohistochemical studies. These results clearly showed

neuroprotective effect of nicotine in experimental model of HD. The clinical

relevance of these findings in HD patients remains unclear and warrants further

studies.

PMID: 16140176 [PubMed - indexed for MEDLINE]

2009 Oct 1;78(7):677-85. Epub 2009 May 9.

Multiple roles for nicotine in Parkinson's disease.

Quik M, Huang LZ, Parameswaran N, Bordia T, Campos C, XA.

The Parkinson's Institute, Sunnyvale, CA 94085, United States.

mquik@...

There exists a remarkable diversity of neurotransmitter compounds in the

striatum, a pivotal brain region in the pathology of Parkinson's disease, a

movement disorder characterized by rigidity, tremor and bradykinesia. The

striatal dopaminergic system, which is particularly vulnerable to

neurodegeneration in this disorder, appears to be the major contributor to these

motor problems. However, numerous other neurotransmitter systems in the striatum

most likely also play a significant role, including the nicotinic cholinergic

system. Indeed, there is an extensive anatomical overlap between dopaminergic

and cholinergic neurons, and acetylcholine is well known to modulate striatal

dopamine release both in vitro and in vivo. Nicotine, a drug that stimulates

nicotinic acetylcholine receptors (nAChRs), influences several functions

relevant to Parkinson's disease. Extensive studies in parkinsonian animals show

that nicotine protects against nigrostriatal damage, findings that may explain

the well-established decline in Parkinson's disease incidence with tobacco use.

In addition, recent work shows that nicotine reduces l-dopa-induced abnormal

involuntary movements, a debilitating complication of l-dopa therapy for

Parkinson's disease. These combined observations suggest that nAChR stimulation

may represent a useful treatment strategy for Parkinson's disease for

neuroprotection and symptomatic treatment. Importantly, only selective nAChR

subtypes are present in the striatum including the alpha4beta2*, alpha6beta2*

and alpha7 nAChR populations. Treatment with nAChR ligands directed to these

subtypes may thus yield optimal therapeutic benefit for Parkinson's disease,

with a minimum of adverse side effects.

PMID: 19433069 [PubMed - indexed for MEDLINE]

http://www.ncbi.nlm.nih.gov/pubmed/19433069?ordinalpos=1 & itool=EntrezSystem2.PEn\

trez.Pubmed.Pubmed_ResultsPanel.Pubmed_SingleItemSupl.Pubmed_Discovery_RA & linkpo\

s=5 & log$=relatedreviews & logdbfrom=pubmed

[Guest guest]

heres another thought based around probelems with bread getting moldy very fast

in a WDB, WHAT HAPPENS TO SUGAR?

3-NP

http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~fE2STH:1

>

> I checked on several know web sites and it's mention as a indoor mold but

basicly a allergen if anything. ARTHRINIUM

> and is this the mycotoxins it produces? 3-NITROPROPIONIC ACID

>

> I was just pretty amased when I started reading about this mold

>

>

[Guest guest]

Jeanine, link doesn't work. Do you have another?

>

> heres another thought based around probelems with bread getting moldy very

fast in a WDB, WHAT HAPPENS TO SUGAR?

> 3-NP

> http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~fE2STH:1

>

[Guest guest]

sorry Barb, not related to my statement, I was just thinking about the

possabilties of how our food also can get contaminated in a WDB. but really just

being in that environment and eating could react with foods we eat while in the

stomach. you breath contaminants, it filters down the back of your throat, you

eat and all this in the tummy, not good.

humm, wonder if I can find info on this arthrinium in sugar being a problem.

something tells me it's a good possability. even still I'm pretty convienced

that there could be several molds and their myco's in WDB's that never get

detected for one reason or another.

hazardous substance database at bottem.

http://ntp.niehs.nih.gov/index.cfm?objectid=E8803E54-BDB5-82F8-F4F502B9D4AC7980

> >

> > heres another thought based around probelems with bread getting moldy very

fast in a WDB, WHAT HAPPENS TO SUGAR?

> > 3-NP

> > http://toxnet.nlm.nih.gov/cgi-bin/sis/search/f?./temp/~fE2STH:1

> >

>

[Guest guest]

heres the basic info on arthrinium

I dont understand why it's reported repeatedly that no known myco's ,

it's obviously been know sence the sugar cane ordeal in china.

the 70's-80's, cant remeber date now.

Arthrinium (ar-thrin'-ee-um) -contaminant, found commonly on dead plants and in

soil. Generally not considered to have much health significance, but one species

is reported to be an allergen. IAQ significance relates to that it will grow in

the same conditions as Stachybotrys (wet cellulose) and amplified amounts in

indoor air could be a warning that conditions do exist for Stachybotrys growth.

no mycotoxins have yet been reported.

Arthrinium: This rapidly growing type of mold usually looks white and has brown

spots, and has a wooly, cotton like texture. Arthrinium is a common contaminant

found in clinical laboratories, but as of yet has not been known to cause any

infections of diseases in humans.

The top four genera of toxigenic, black mold are:

Stachybotrys, Aspergillus, Penicillium, and Fusarium. Species of Aspergillus and

Penicillium look a great deal alike, and are quite common in most areas around

the country, while Stachybotrys and Fusarium turn up more in rural areas (farm

land, barns) where there are greater odds of cellulose material remaining damp

for long periods of time

[Guest guest]

EMSL /ARTHRINIUM/ 2 TOXINS PRODUCED /SUBSTRATES IN INDOOR ENVIRONMENT-CELLULOSE

CONTAINING MATERIALS

http://www.emsl.com/index.cfm?nav=Pages & ID=155

Arthrinium: A common saprophyte that is frequently

found on decaying plants or grass, also found in soil. A

reported allergen with no associated diseases related to

toxic effects. This mold can be found everywhere both

outside and indoors.

http://www.digitaldiagnosticsystems.com/Mold%20Glossary06.pdf

[Guest guest]

This mycotoxin is use to disrupt mitochondrial function.

To address these issues, we used an established model of mitochondrial

dysfunction induced by local application of 3-nitropropionic acid (3-NP), an

irreversible inhibitor of succinate dehydrogenase (SDH), to produce

mitochondrial dysfunction

Disruption of the mitochondrial energetic function

SDH was selected as a target enzyme for inhibition of the mitochondrial energy

production

SDH activity was inhibited by 3-NP, an irreversible SDH inhibitor produced on

moldy crops by the fungus Arthrinium sp. 3-NP (Sigma, USA) was dissolved in a

normal artificial perilymph (142 mM NaCl, 5.37 mM KCl, 1.47 mM MgCl2, 2 mM

CaCl2, and 10 mM HEPES) to generate a stock solution (400 mM). The stock

solution was stored at a temperature of -20 °C for less than one month. Before

each application, the stock solution was diluted with the artificial perilymph

to produce a working concentration (20 or 50 mM).

1999 3-Nitropropionic Acid (3-NPA) Produces Hypothermia and Inhibits

Histochemical Labeling of Succinate Dehydrogenase (SDH) in Rat Brain

http://www.springerlink.com/content/l234rt851174021r/

[Guest guest]

Terpestacin (a new antibiotic)

http://cat.inist.fr/?aModele=afficheN & cpsidt=4720321

1987 Nov 5-11;330(6143):74-7.

Interference with HIV-induced syncytium formation and viral infectivity by

inhibitors of trimming glucosidase.

Gruters RA, Neefjes JJ, Tersmette M, de Goede RE, Tulp A, Huisman HG, Miedema F,

Ploegh HL.

Central Laboratory, Netherlands Red Cross Blood Transfusion Service, University

of Amsterdam.

Human immunodeficiency virus (HIV), the causative agent of AIDS, infects human

lymphocytes and monocytes. An interaction between the viral envelope gp 120 and

CD4 protein is required to initiate an infectious cycle. HIV infection in vitro

induces syncytium formation by cell-to-cell fusion; this aspect of viral

cytopathogenicity is even more dependent on gp120-CD4 interactions. That gp120

is extremely heavily glycosylated (31-36 N-linked glycans per molecule),

suggests involvement of N-linked glycans in the gp120-CD4 interaction. We

therefore investigated the effects of castanospermine, 1-deoxynojirimycin (dNM)

and 1-deoxymannojirimycin (dMM), three trimming glycosidase inhibitors which

perturb N-linked glycan structure, on induction of the formation of syncytium

between HIV-infected and CD4-expressing cells. The glucosidase inhibitors

castanospermine and dNM, but not the mannosidase inhibitor dMM, inhibited

syncytium formation and interfered with infectivity. The potential of

glucosidase inhibitors as anti-HIV therapeutic agents deserves further

investigation, especially because dNM and related compounds show little toxicity

in vitro and in vivo.

PMID: 2959866 [PubMed - indexed for MEDLINE

http://www.ncbi.nlm.nih.gov/pubmed/2959866

[Guest guest]

so, can someone explain to me why arthrinium is lised with most articles as

being rather harmless, when it's known to prouduce 2 toxins that dont appear to

be harmless at all?

in the article of the nasal air tester it stated something along the lines that

the spores being pretty small might be more airborne.

some state that it basicly may be growing right along with stachy.

like stachy doesn't sometimes get detected because the spores are heavy, might

arthrinium not get detected because they are lighter and more airborne?

whats the chances that this mold is pretty well ignored because it's labeled as

being pretty harmless?

did the the attn. that stachy got somehow take away from this mold getting the

reconition it maybe should have got?

sounds like the possability of it being in the WDB invironment would be just as

good as stachy.

>

> EMSL /ARTHRINIUM/ 2 TOXINS PRODUCED /SUBSTRATES IN INDOOR

ENVIRONMENT-CELLULOSE CONTAINING MATERIALS

> http://www.emsl.com/index.cfm?nav=Pages & ID=155

>

>

> Arthrinium: A common saprophyte that is frequently

> found on decaying plants or grass, also found in soil. A

> reported allergen with no associated diseases related to

> toxic effects. This mold can be found everywhere both

> outside and indoors.

> http://www.digitaldiagnosticsystems.com/Mold%20Glossary06.pdf

>