Tissue 65Zinc translocation in a rat model of chronic aldosteronism.

Abstract

Zinc, an essential micronutrient, is involved in wound healing. The hypozincemia seen with chronic aldosteronism is associated with enhanced fecal and urinary excretory Zn losses, and its tissue distribution is less certain. This study monitored tissue 65Zn distribution in uninephrectomized rats at weeks 1 and 4 of aldosterone/salt treatment (ALDOST). Plasma and tissue total radionucleotide uptake was determined by calculating its mean radioactivity at 1, 4, 8, 24, and 48 hours after intravenous 65Zn administration and where respective area under the concentration-time curves (AUC) were determined by the linear trapezoidal rule and expressed as a tissue:plasma AUC ratio. Examined tissues included: (1) injured heart and kidney in response to ALDOST and incised skin; (2) noninjured liver, skeletal muscle, and spleen sites of stress-linked Zn uptake; and (3) bone, a major storage and release site when Zn homeostasis is threatened. In comparison with age-matched and gender-matched controls, the following were found with week 1 and 4 ALDOST: (1) reduced plasma 65Zn; (2) an accumulation of 65Zn in heart and kidneys, where a well-known vasculopathy involves intramural vessels, and in incised skin at week 1; (3) an organ-specific increase in tissue 65Zn in liver, in keeping with upregulated metallothionein expression, skeletal muscle, and spleen; and (4) a fall in bone and healed skin Zn at week 4. Thus a wide-ranging disturbance in Zn homeostasis appears during ALDOST to include its translocation from plasma to injured heart, kidneys, and skin and noninjured liver, skeletal muscle, and spleen together with a resorption of stored Zn in bone at week 4. Zinc dyshomeostasis is an integral feature of chronic aldosteronism.