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Blood, Vol. 94 No. 11 (December 1), 1999:
pp. 3906-3914
Defective Recovery and Severe Renal Damage After Acute Hemolysis in
Hemopexin-Deficient Mice
Emanuela Tolosano,
Emilio Hirsch,
Enrico Patrucco,
Clara Camaschella,
Roberto Navone,
Lorenzo Silengo, and
Fiorella Altruda
From the Department of Genetics, Biology and Biochemistry, Department
of Clinical and Biological Sciences, and Department of Biomedical
Sciences and Human Oncology, University of Turin, Turin, Italy.
Hemopexin (Hx) is a plasma glycoprotein mainly expressed in liver
and, less abundantly, in the central and peripheral nervous systems. Hx
has a high binding affinity with heme and is considered to be a major
transport vehicle of heme into the liver, thus preventing both
heme-catalyzed oxidative damage and heme-bound iron loss. To determine
the physiologic relevance of heme-Hx complex formation, Hx-deficient
mice were generated by homologous recombination in embryonic stem (ES)
cells. The Hx-deficient mice were viable and fertile. Their plasma iron
level and blood parameters were comparable to those of control mice and
they showed no evidence of tissue lesions caused by oxidative damage or
abnormal iron deposits. Moreover, they were sensitive to acute
hemolysis, as are wild-type mice. Nevertheless, Hx-null mice recovered
more slowly after hemolysis and were seen to have more severe renal
damage than controls. After hemolytic stimulus, Hx-deficient mice
presented prolonged hemoglobinuria with a higher kidney iron load and
higher lipid peroxidation than control mice. Moreover, Hx-null mice
showed altered posthemolysis haptoglobin (Hp) turnover in as much as Hp
persisted in the circulation after hemolytic stimulus. These data
indicate that, although Hx is not crucial either for iron metabolism or
as a protection against oxidative stress under physiologic conditions,
it does play an important protective role after hemolytic processes.
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