<monty1945 DeleteThis @lycos.com> wrote in message
news:1174336707.372206.18120@o5g2000hsb.googlegroups.com...
> I read a few reports but none mentioned exactly what is the toxin.
> Anyone know or have an idea?
......At first I was wondering if it was a problem with the bag packaging,
but since actual cans of similar food seems to be also affected (unless
they're pulling stuff off the shelf due to caution) my guess is that it's a
fungal toxin (mycotoxin) of wheat if the wheat gluten is the cause. The one
that causes kidney damage is ochratoxin A. I'm sort of surprised though
that they haven't nailed it down if its a mycotoxin as there's tests
available that should be fairly quick.
http://www.mycotoxins.org/
Basic fact sheets for each mycotoxin. Look at Ochratoxin A.
http://www.inchem.org/documents/ehc/ehc/ehc011.htm
"The morphological changes in the kidneys in cases of mycotoxic porcine
nephropathy are characterized by degeneration of the proximal tubules,
followed by atrophy of the tubular epithelium, interstitial fibrosis in the
renal cortex, and hyalinization of some glomeruli (Elling & Moller, 1973)
"Acute and chronic effects. The acute and chronic effects of ochratoxins in
experimental animals have been reviewed by Chu (1974a), Harwig (1974), and
Krogh (1976a). Different species vary in their susceptibility to acute
poisoning by ochratoxin A, with LD50 values ranging from 3.4 to 30.3 mg/kg
(Table 24). When administered orally to rats, the female is more sensitive
to ochratoxin A than the male. The kidney is the target organ, but changes
in the liver have also been noted during studies of acute
effects."...........
"The lesions observed in field cases of mycotoxic porcine nephropathy
(section 4.1.4.1) have been reproduced by feeding diets containing levels of
ochratoxin A identical to those encountered in naturally contaminated
products (section 4.1.2.2). Thus 39 pigs fed rations containing ochratoxin A
at levels ranging from 200-4000 µg/kg developed nephropathy after 4 months
at all levels of exposure (Krogh et al., 1974). Changes in renal function
were characterized by impairment of tubular function, indicated
particularly by a decrease in TmPAH/CIna and reduced ability to produce
concentrated urine. These functional changes corresponded well with the
changes in renal structure observed at all exposure levels including atrophy
of the proximal tubules, and interstitial cortical fibrosis. Sclerotized
glomeruli were also observed in the group receiving the highest dose of
ochratoxin A of 4000 µg/kg feed. No other organ or tissue exhibited any
changes.".............
"In pigs and dogs given high peroral doses, corresponding to feed levels of
more than 5-10 mg/kg (levels rarely found in nature) extrarenal effects, in
addition to renal lesions, were observed, involving the liver, intestine,
spleen, lymphoid tissue, and leukocytes (Szczech et al., 1973a,b,c). Three
groups of rats, each consisting of 15 animals were exposed to feed levels of
ochratoxin A ranging from 0.2 to 5 mg/kg for 3 months. Renal damage in the
form of tubular degeneration was observed at all dose levels (Munro et al.,
1974).".......
" The toxic effects of ochratoxin A have been studied extensively in a
variety of experimental animals. All the animals studied so far have been
susceptible to orally administered ochratoxin A, but to various degrees, as
indicated by the range of LD50 values (Table 24). At high levels of
ochratoxin A, changes were found in the kidneys and also in other organs and
tissues. However, only renal lesions were observed at exposure levels
identical to those occurring environmentally. The renal lesions included
degeneration of the tubules, interstitial fibrosis, and, at later stages,
hyalinization of glomeruli, with impairment of tubular function as a prime
manifestation. Feed levels as low as 200 µg/kg produced renal changes in the
course of 3 months in rats and pigs. Field cases of ochratoxin A-induced
nephropathy are regularly encountered in pigs and poultry. Ochratoxin A is
teratogenic in the mouse, rat, and hamster...............
Ochratoxin A (OTA) also seems to increase it's own uptake into the body
through altering the intestinal epithelium/mucosal membrane.
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_ui
ds=11578148&dopt=Abstract
Toxicol Appl Pharmacol. 2001 Oct 1;176(1):54-63.
The mycotoxin ochratoxin A alters intestinal barrier and absorption
functions but has no effect on chloride secretion.
Maresca M, Mahfoud R, Pfohl-Leszkowicz A, Fantini J.
Faculte des Sciences St-Jerome, Institut Mediterraneen de Recherche en
Nutrition, 13397 Marseille Cedex 20, France.
"In particular, OTA affected the protein content of plasma membrane
microdomains, which are known to regulate tight junction assembly and
intestinal transport activity. Taken together, these data showed that OTA
alters both barrier and absorption functions of the intestinal epithelium."
It's also largely dumped out of the system through conjugation of bile
salts. If a cat was low on taurine (which cats use exclusively to conjugate
bile) it might get damaged kidneys faster as it wouldn't be removed from the
blood stream.
http://jpet.aspetjournals.org/cgi/content/abstract/279/3/1507
Volume 279, Issue 3, pp. 1507-1513, 12/01/1996
Copyright © 1996 by American Society for Pharmacology and Experimental
Therapeutics
Uptake of the mycotoxin ochratoxin A in liver cells occurs via the cloned
organic anion transporting polypeptide
M Kontaxi, U Echkardt, B Hagenbuch, B Stieger, PJ Meier and E Petzinger
Institute of Pharmacology and Toxicology, Justus-Liebig-University, Giessen,
Germany.
"Ochratoxin A (OTA) is a mycotoxin produced by mold. It mainly causes
nephropathies in humans and domestic animals as a major pathogenic
contaminant of cereals and animal feed. Upon p.o. uptake and intestinal
absorption, a large part of OTA is taken up by hepatocytes and eliminated
into bile."
It appears the damage of the kidney is from inhibition of a gene that turns
on anti-oxidant defenses in a detoxification pathway.
http://toxsci.oxfordjournals.org/cgi/content/abstract/96/1/30
Reduction in Antioxidant Defenses may Contribute to Ochratoxin A Toxicity
and Carcinogenicity
The sentence below helps make sense of the article above.
http://www.jbc.org/cgi/content/abstract/279/22/23052
J. Biol. Chem., Vol. 279, Issue 22, 23052-23060, May 28, 2004
Transcription factor NF-E2-related factor 2 (Nrf2) regulates the induction
of Phase II detoxifying enzymes as well as anti-oxidative enzymes.
In the case of aflatoxin exposure, adequate levels of Vit A, protein, and
selenium all protect the body against effects of aflatoxin
AFLATOXIN
http://www.inchem.org/documents/ehc/ehc/ehc011.htm
Scroll down to Table 12: The effects of dietary protein and vitamin B12 on
aflatoxin-induced liver changes
Table 13 and 14 - Vitamin A and aflatoxin
........so who gets sick probably depends on the amount eaten (eats same
thing every day), how long they were eating it, how good the rest of the
diet is (adequate and even supplemental levels of some nutrients) and
whether or not there's already kidney damage and if the intestines and gall
bladder are in good working order to begin with.
.......There's not a lot of info on cats and dogs, but ochratoxin A seems to
cause kidney damage across all mammalian species. Cats are more sensitive
to a lot of chemicals than are dogs.
buglady
take out the dog before replying
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