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The biological half-life of 137Cs and its organ distribution were investigated in mice fed various potassium-deficient diets. The biological half-life, which was 6.1 days in mice receiving the normal level of potassium, became longer as the dietary potassium content decreased, and 137Cs was hardly excreted from the body when dietary potassium content was restricted to 200 mg/kg or less. The muscle showed the highest concentration of 137Cs in both mice that had sufficient amounts of potassium and those that were potassium-deficient. Clearance of 137Cs from tissues was generally suppressed when mice were fed a potassium-deficient diet, but the relative distribution pattern of 137Cs was not affected by dietary potassium content. These results suggest that dietary potassium intake, which may vary with eating habits, affects the biological half-life of 137Cs in humans.

The prostate is an accessory sex organ that secretes essential components of semen. High levels of Zn are found both in the prostate and its secretion. In the present study, the effects of environmental stress on zinc levels in the prostate were examined in Wistar male rats exposed to tributyltin chloride (TBTC), an environmental toxicant, by inductively coupled argon plasma–mass spectrometry (ICP-MS) for determination of Zn concentration in lobe-dissectioned specimens and micro-PIXE analysis for determination of site-specific distribution of Zn in prostatic sections. A single oral administration of TBTC to rats at a dose of 90 μmol/kg resulted 14 days later in a decrease in the Zn level in the dorsolateral prostate but not the ventral prostate. The TBTC did not affect the weight of the prostate tissue. Micro-PIXE imaging found Zn both in the lumen and the epithelium of the lateral prostatic tubules. PIXE spot analysis revealed that the epithelium of the control rat contained levels of Zn 4–fold higher than in the lumen and that Zn in the epithelium decreased selectively after TBTC exposure.

Iron accumulation in the basal ganglia and spheroid formation are pathological hallmarks of Hallervorden-Spatz disease (HS). Since an overaccumulation of iron (iron thesaurosis) that exceeds the binding capacity of ferritin could cause oxidative damage, we studied the possible role of oxidative stress in the pathogenesis of HS. The basal ganglia and spinal cord from patients with HS were investigated at autopsy, using histochemistry for iron and immunohistochemistry for Cu/Zn superoxide dismutase (SOD1), Mn superoxide dismutase (SOD2) and ferritin. SOD1-like immunoreactivity (IR), SOD2-IR and ferritin-IR occurred frequently in spheroids observed in the basal ganglia, and associated iron accumulation indicated the possible existence of increased oxidative stress in HS patients. Spheroids in the spinal cord showed intense SOD1-IR and SOD2-IR in HS, in sharp contrast with the occasional weak SOD1-IR and SOD2-IR observed in spheroids from patients with amyotrophic lateral sclerosis (ALS). Neither increased ferritin-IR nor iron accumulation were observed in spinal spheroids from HS and ALS patients. These data may suggest that, at least in the spinal cord, SOD1-IR and SOD2-IR in spheroids in HS patients do not result from oxidative stress directly related to iron accumulation.

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