Biol Res Nurs. 2007 Apr;8(4):300-4.The dose-dependent effects of
chronic iron overload on the production of oxygen free radicals and
vitamin e concentrations in the liver of a murine model.McCullough KD,
Bartfay WJ.
Nursing Faculty, Nipissing University, North Bay, Ontario, Canada.

Genetic disorders of iron metabolism such as primary and secondary
hemochromatosis affect thousands of individuals worldwide and are
major causes of liver dysfunction, morbidity, and mortality. Although
the exact mechanism of hepatic injury associated with these genetic
disorders is not fully understood, the propagation of excess
concentrations of iron-catalyzed oxygen free radicals (OFRs) may play
a role. The authors hypothesized that chronic iron burden would result
in dose-dependent (a) increases in hepatic iron stores, (b) increases
in hepatic OFR-mediated hepatic cellular injury as quantified by the
cytotoxic aldehydes malondialdehyde (MDA) and hexanal, and (c)
decreases in protective antioxidant reserve status as quantified by
plasma vitamin E (alpha-tocopherol) levels in a murine model. Twenty
B(6)D(2)F1 male mice were randomized to the (a) saline control (0.05
mL intraperiotoneal [i.p.]/mouse/day, n = 5), (b) 100 mg total iron
burden (n = 5), (c) 200 mg total iron burden (n = 5), or (d) 400 mg
total iron burden (n = 5) group. Iron burden was achieved by daily
injections of iron dextran (Imferon, 0.05 mL i.p./mouse/day). In
comparison to control mice and in support of the hypothesis, the
authors observed significant dose-dependent increases in total hepatic
iron burden (p < .001) with corresponding increases in MDA and hexanal
concentrations (p < .001) and decreases in the protective plasma
antioxidant vitamin E (p < .001). These findings suggest that iron-
catalyzed OFR-mediated damage may play a role in damaging the liver in
chronic states of iron burden.

PMID: 17456591 [PubMed - in process]

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