mycotoxin transporters

[Guest guest]

Research article summary (published 3 Mar 2008):

Free Full Text!

See links below

Interactions of organic anion transporters and organic cation transporters with

mycotoxins.

Full Abstract

Mycotoxins are secondary metabolites of moulds that which exert adverse effects

in humans and animals. It is known that direct cellular toxicity is often

associated with increased cellular accumulation of toxic compounds, and membrane

transport may be the first fundamental stage in the development of the

cytotoxicity. To elucidate the entry pathway for mycotoxins into cells, we have

investigated the interactions of human and rat organic anion transporters

(hOATs/rOats) and human organic cation transporters (hOCTs) with mycotoxins

using cells stably expressing hOATs/rOats/hOCTs. The mycotoxins tested were

aflatoxin B1, alpha-zearalenol, citrinin, citrioveridine, cyclopiazonic acid,

fumonisin B1, gliotoxin, patulin, penicillic acid, rubratoxin B, and

zearalenone. These mycotoxins inhibited organic anion uptake mediated by

hOAT1-4, and organic cation uptake mediated by hOCT1-2. By comparing the IC(50)

values of mycotoxins for hOATs, it was found that hOAT1 and hOAT3 exhibited

higher affinity interactions with mycotoxins than hOAT2 and hOAT4. There was no

interspecies difference between humans and rats for the interactions of OATs

with mycotoxins except that of OAT3 with rubratoxin B. Finally, we observed that

hOAT1-4 and hOCT1-2 mediated the uptake of aflatoxin B1. In conclusion, hOATs

and hOCTs interacted with various mycotoxins. Considering the localization of

hOATs/rOats and hOCTs, it was suggested that these transporters were the

possible entrance pathway for mycotoxins in kidney and liver, leading to the

induction of adverse effects in humans and rats.

http://www.find-health-articles.com/rec_pub_18319568-interactions-organic-anion-\

transporters-organic-cation-transporters.htm

[Guest guest]

anyone else seeing how myoco's and other toxins involve a seperate pathway in

the body than say some bacteria's and mold spores/non-toxic products of spores

anyway,or the infection causes of mold.

humm, dont know really how to state that properly but theres two different

pathways involved here, with detection,tranporting,effects/organ damage and how

the body deals with both. several myco's site apoptosis vs. necrosis but I've

also read where some myco's caused apoptosis the first week and necrosis after

that plus apoptosis. it's like they all may start and end at the same but two

diffent pathways involved in the middle.

the danger signal theory,amaseing. I have to wonder how that theory

may have been looked at in the 90's by several opposers of getting toxic mold

exposure reconized. very possably several that already knew because of many

years of already dealing with toxic molds in certain commodities that they were

heavily invested in.

[Guest guest]

2006;100(5):411-26.

Organic anion transporter family: current knowledge

http://www.ncbi.nlm.nih.gov/pubmed/16799257

following the more resent by year to the right,related articles. gives more

info.

this is kindof one of the reasons I full like it's more about total toxin body

load and dose than masking and unmasking. or more so that dose/total body toxin

load plays a role in unmasking and that even some med's

could hinder the abiality to " unmask " and it really is all about the dose. dose

with exposure, dose in the body.

just my thoughts.

>

> Research article summary (published 3 Mar 2008):

>

> Free Full Text!

> See links below

> Interactions of organic anion transporters and organic cation transporters

with mycotoxins.

>

> Full Abstract

> Mycotoxins are secondary metabolites of moulds that which exert adverse

effects in humans and animals. It is known that direct cellular toxicity is

often associated with increased cellular accumulation of toxic compounds, and

membrane transport may be the first fundamental stage in the development of the

cytotoxicity. To elucidate the entry pathway for mycotoxins into cells, we have

investigated the interactions of human and rat organic anion transporters

(hOATs/rOats) and human organic cation transporters (hOCTs) with mycotoxins

using cells stably expressing hOATs/rOats/hOCTs. The mycotoxins tested were

aflatoxin B1, alpha-zearalenol, citrinin, citrioveridine, cyclopiazonic acid,

fumonisin B1, gliotoxin, patulin, penicillic acid, rubratoxin B, and

zearalenone. These mycotoxins inhibited organic anion uptake mediated by

hOAT1-4, and organic cation uptake mediated by hOCT1-2. By comparing the IC(50)

values of mycotoxins for hOATs, it was found that hOAT1 and hOAT3 exhibited

higher affinity interactions with mycotoxins than hOAT2 and hOAT4. There was no

interspecies difference between humans and rats for the interactions of OATs

with mycotoxins except that of OAT3 with rubratoxin B. Finally, we observed that

hOAT1-4 and hOCT1-2 mediated the uptake of aflatoxin B1. In conclusion, hOATs

and hOCTs interacted with various mycotoxins. Considering the localization of

hOATs/rOats and hOCTs, it was suggested that these transporters were the

possible entrance pathway for mycotoxins in kidney and liver, leading to the

induction of adverse effects in humans and rats.

>

>

http://www.find-health-articles.com/rec_pub_18319568-interactions-organic-anion-\

transporters-organic-cation-transporters.htm

>