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Sephadex G-100 chromatography of rat liver supernatant after addition of [125I]T3 revealed four peaks of protein-bound radioactivity in the void volume, albumin, ligandin, and Z-containing regions, respectively. The peaks were identified by cochromatography of BSP and [125I]T3 and immonodiffusion with antiratligandin IgG and antirat Z IgG. Binding of [125I]T4 to rat liver supernatant occurred in void volume, albumin, and Z regions only. Studies in vivo reveal a pattern of [125I]T3 binding to rat liver supernatant fractions quantitatively different from that observed in vitro. [125I]T4 binding to liver supernatant fractions in vivo occurred in all four peaks. BSP or bilirubin added to liver supernatant decreased T3 and T4 binding by each fraction. Flavaspidic acid inhibited binding of T3 and T4 to albumin, ligandin, and Z protein. Phenobarbital pretreatment of rats increased binding of T3 by ligandin and of T4 by albumin-containing fractions. Circular dichroism studies with purified rat liver ligandin suggest that T3 and T4 bind competitively to the same site as does bilirubin; the association constants of T3 and T4 for ligandin are 10(6) and 10(5) M-1, respectively. T4 was bound only by purified ligandin and not by ligandin in liver supernatant. To determine whether unconjugated bilirubin interferes with hepatic uptake of T3, [125I]T3 was administered to icteric homozygous and phenotypically normal heterozygous Gunn rats. Hepatic uptake and supernatant binding [125I]T3 were significantly reduced in homozygous Gunn rats. Hepatic uptake of [125I]T3 was also reduced in vivo by infusion of BSP with or without flavaspidic acid. BSP infusion abolished [125I]T3 binding to ligandin; BSP and flavaspidic acid abolished binding to ligandin and Z. These observations suggest that ligandin and Z protein are thyroid hormone binding proteins in rat liver cytosol and may influence the net flux of iodothyronies from plasma into the liver.

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Six patients with varying degrees of renal insufficiency developed severe hyperkalemia following hepatic necrosis. The hyperkalemia was seen prior to or concomitant with marked elevations in hepatic enzymes. The basis of the liver disease appeared to involve congestive heart failure and/or hypotension. Necrotic liver cells released intra-cellular potassium into the blood of patients who were unable to handle the additional potassium load because of renal insufficiency and metaboic acidosis. Furthermore, a shift of potassium into the intracellular space is impaired in uremics by defective Na-K ATPase activity, possibly induced by uremic toxins. The 3 diabetic patients in our series may additionally have had aldosterone deficiency leading to impaired cellular potassium uptake.

An ethnic or racial division of labor exists in a society in which ethnic or racial groups have distinctive concentrations or specializations in particular lines of work. Ethnic/racial divisions of labor may arise through relatively benign labor market sorting processes, or they may be the result of systematic acts of bigotry and discrimination, often with state sanction. Regardless of how they arise, ethnic/racial divisions of labor can be observed and traced over time, and they can have measurable effects on social and political dynamics within societies.