So eating the white meat such as chicken or fish from those iron
plates should be relatively safe compared to the red meat such as
beef? <<

Nooo .. anything that causes one to absorb MORE IRON THAN REQUIRED is
in the file called .. increased iron.
There is no file for meat in not increased iron.
Meat and plants are different in that plants do not contain blood.
Blood iron causes iron to be absorbed at a higher rate at all times of
iron status.
When one has enough iron on board one downregulates the amount of iron
one absorbs.
When one eats blood / heme iron the iron is absorbed whether you need
it
or not and this leads to a autoimmune like type disease somewhat like
porphyria.

"Ascorbate suppresses hepatic URO accumulation at low, but not high
hepatic iron levels"

This shows when the iron gets to a 'certain point' .. BOOM ..

"Was not observed until a high hepatic iron threshold was exceeded"

It shows it can be controlled by targeting the iron with diet and / or
DIRECT iron targeting.

One might argue this is not an ALS mouse.
Iit does concern the uroporphyrin.
In that uroporphyrin induces an autoimmune response / autoimmune like
response.

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 havesuggested a role for ascorbate (AA) in
suppressing uroporphyria inAA-requiring rats (in the absence of excess
iron), the present studyinvestigated whether AA could suppress
uroporphyria produced byexcess 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 maintainnear normal hepatic AA levels or a lower intake (75
ppm) that resulted in70% lower hepatic AA levels.
The higher AA intake suppressed hepatic URO accumulation in the
absence of administered iron, but not when irondextran (300-500 mg Fe/
kg) was administered.
This effect of iron wasnot 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.

(HEPATOLOGY2007;45:187-194.).

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

Effect of an oral iron chelator or iron-deficient diets on
uroporphyria in a murine model of porphyria cutanea tarda.
Hepatology. 2007 Sep 13;
Gorman N, Zaharia A, Trask HS, Szakacs JG, Jacobs NJ, Jacobs JM,
Balestra D, Sinclair JF, Sinclair PR.
Veterans Affairs Medical Center, White River Junction, VT.

Porphyria cutanea tarda is a liver disease characterized by elevated
hepatic iron and excessive production of uroporphyrin (URO).
Phlebotomy is an effective treatment that probably acts by reducing
hepatic iron.
Here we used Hfe(-/-) mice to compare the effects on
hepatic URO accumulation of two different methods of hepatic iron
depletion: iron chelation using deferiprone (L1) versus iron-
deficient diets.
Hfe(-/-) mice in a 129S6/SvEvTac background were fed 5-
aminolevulinic acid (ALA), which results in hepatic URO accumulation,
and increasing doses of L1 in the drinking water. Hepatic URO
accumulation was completely prevented at low L1 doses, which partially
depleted hepatic nonheme iron. By histological assessment, the
decrease in hepatic URO accumulation was associated with greater
depletion of iron from hepatocytes than from Kupffer cells.
The L1 treatment had no effect on levels of hepatic cytochrome P4501A2
(CYP1A2).
L1 also effectively decreased hepatic URO accumulation in
C57BL/6 Hfe(-/-) mice treated with ALA and a CYP1A2 inducer. ALA-
treated mice maintained on defined iron-deficient diets, rather than
chow diets, did not develop uroporphyria, even when the animals were
iron-supplemented either directly in the diet or by iron dextran
injection.
Conclusion:
The results suggest that dietary factors other than iron are involved
in the development of uroporphyria and that a modest depletion of
hepatocyte iron by L1 is sufficient to prevent URO accumulation.
(HEPATOLOGY 2007.).

PMID: 17854053