Biological efficacy of partial hepatectomy and hepatopoietin in long-term selenium-deficient mice.

After partial hepatectomy the normal low proliferation rate of hepatocytes increases dramatically. This is based on a feed-back system whose central link is a liver cell proliferation hormone, the so-called hepatopoietin. This glycoprotein is organ-specific but not species-specific, i.e. an extract from rats is also active in mice. In order to examine the influence of selenium on liver cell proliferation, male albino NMRI mice were fed a selenium-deficient diet containing less than 10 ppb Se for at least 2 months (Se-). In the plasma protein profile and in the basic DNA synthesis rate of Se(-)-animals, no significant changes were observed compared to controls. However, liver cell proliferation induced by hepatopoietin or by partial hepatectomy was increased about 3-fold in Se-deficient mice. We assume a compensated metabolic Se-deficiency state in mice under these nutritional conditions, which leads to expression of enhanced metabolic capacity when induced by stress.