<<snip>>
chemicals, iron and ALA can act independently, but also together, to
cause porphyria in susceptible individuals.
<<snip>>

<<snip>>
test MCS patients for **increased porphyrin**
<<snip>>

Uroporphyria induced by 5-aminolaevulinic acid alone in Ahrd SWR mice.
Constantin D, Francis JE, Akhtar RA, Clothier B, Smith AG
Biochem Pharmacol. 1996 Nov 8; 52(9): 1407-13

In mice, depression of hepatic uroporphyrinogen decarboxylase (UROD)
leading to porphyrin accumulation (uroporphyria) occurs with
chlorinated ligands of the aryl hydrocarbon (AH) receptor especially
after iron overload. However, in the absence of chlorinated ligands,
iron itself will eventually cause uroporphyria, but this response is
not associated with the Ahr genotype. These effects are potentiated by
administration of the haem precursor 5-aminolaevulinate (ALA). The aim
of this study was to investigate the effects of ALA alone. Prolonged
administration of 2 mg ALA/mL in the drinking water to SWR mice also
led to decarboxylase insufficiency (11% of control) and uroporphyria by
8 weeks, whereas DBA/2 mice did not show reduced enzyme activity. Both
strains are considered AH nonresponsive and analysis of the Ahr gene
using restriction fragment length polymorphism was consistent with SWR,
like DBA/2, possessing the Ahrd allele. Exposure of isolated
hepatocytes to ALA (150-500 microM) for up to 48 hr showed a
significant accumulation of both uroporphyrin and coproporphyrin in the
medium, which for uroporphyrin particularly was significantly greater
with SWR than with DBA/2 cells. Basal in vivo CYP1A2 activity, measured
as microsomal methoxyresorufin dealkylation, was significantly greater
in SWR than in DBA/2 mice (1.3-fold), but it was unclear whether this
was sufficient to explain the marked difference in sensitivities of the
two strains. Despite SWR mice being AH nonresponsive, uroporphyria and
decarboxylase depression after an initial iron overload and ALA for 3
weeks were greatly potentiated by a single dose (100 mg/kg) of
hexachlorobenzene (a weak AH ligand). The results demonstrate that
there is a genetic difference in mice independent of the Ahr genotype
and response to iron, which influences the susceptibility to
ALA-induced uroporphyria. Thus chemicals, iron and ALA can act
independently, but also together, to cause porphyria in susceptible
individuals.

------------------------------------------------------------------------------------------------------------------

Multiple Chemical Sensitivitity (MCS)Multiple Chemical Sensitivity is
the name given to a syndrome in which a ... test MCS patients for
**increased porphyrin** content in urine and stool samples. ...
www.ei-resource.org/mcs.asp - 87k - Dec 25, 2006 - Cached - Similar
pages

------------------------------------------------------------------------------------------------------------------

<<snip>>
ascorbate suppresses hepatic URO accumulation at low, but not high
hepatic iron levels
<<snip>>

Effect of iron and ascorbate on uroporphyria in ascorbate-requiring
mice as a model for porphyria cutanea tarda.
Gorman N, Zaharia A, Trask HS, Szakacs JG, Jacobs NJ, Jacobs JM,
Balestra D, Sinclair JF, Sinclair PR
Hepatology. 2006 Dec 22; 45(1): 187-194

Excess hepatic iron is known to enhance both porphyria cutanea tarda
(PCT) and experimental uroporphyria. Since previous studies have
suggested a role for ascorbate (AA) in suppressing uroporphyria in
AA-requiring rats (in the absence of excess iron), the present study
investigated whether AA could suppress uroporphyria produced by excess
hepatic iron. Hepatic URO accumulation was produced in AA-requiring
Gulo(-/-) mice by treatment with 3,3',4,4',5-pentachlorbiphenyl, an
inducer of CYP1A2, and 5-aminolevulinic acid. Mice were administered
either sufficient AA (1000 ppm) in the drinking water to maintain near
normal hepatic AA levels or a lower intake (75 ppm) that resulted in 70

% lower hepatic AA levels. The higher AA intake suppressed hepatic URO
accumulation in the absence of administered iron, but not when iron
dextran (300-500 mg Fe/kg) was administered. This effect of iron was
not due to hepatic AA depletion since hepatic AA content was not
decreased. The effect of iron to prevent AA suppression of hepatic URO
accumulation was not observed until a high hepatic iron threshold was
exceeded. At both low and high AA intakes, hepatic malondialdehyde
(MDA), an indicator of oxidative stress, was increased three-fold by
high doses of iron dextran. MDA was considerably increased even at low
iron dextran doses, but without any increase in URO accumulation. The
level of hepatic CYP1A2 was unaffected by either AA intake. Conclusion:

In this mouse model of PCT, AA suppresses hepatic URO accumulation at
low, but not high hepatic iron levels. These results may have
implications for the management of PCT. (HEPATOLOGY 2007;45:187-194.).

------------------------------------------------------------------------------------------------------------------

The iron loading diseases .. hemochromatosis and hepatitis C .. may
CAUSE .. porphyria ..

Sooo .. eating .. meat .. that highly absorbable form of iron FOUND in
meat .. then raises iron levels .. and therefore may CAUSE ..
porphyria.

http://exchange.healthwell.com/news.cfm?news=1746

<<snip>>
"it is probable that a chronically high intake of heme iron can lead
to high body iron stores and thus may elevate the risk of diabetes,"
the authors said. "
<<snip>>

http://en.wikipedia.org/wiki/Porphyria

<<snip>>
Some liver diseases may cause porphyria even in the absence of genetic
predisposition. These include hemochromatosis and hepatitis C.
Treatment of iron overload may be required.
<<snip>>

Who loves ya.
Tom

Jesus Was A Vegetarian!
http://jesuswasavegetarian.7h.com

Man Is A Herbivore!
http://tinyurl.com/a3cc3

DEAD PEOPLE WALKING
http://tinyurl.com/zk9fk