Bank voles (Clethrionomys glareolus) and laboratory strains of house mice (Mus musculus BALB and C57BL) were relocated into enclosures in a highly contaminated area of the Red Forest near the Chornobyl (Ukraine) Reactor 4 to evaluate the uptake rates of 137Cs and 90Sr from abiotic sources. Mice were provided with uncontaminated food supplies, ensuring that uptake of radionuclides was through soil ingestion, inhalation, or water. Mice were sampled before introduction and were reanalyzed every 10 d for 137Cs uptake. Levels of 90Sr were assessed in subsamples from the native populations and in experimental animals at the termination of the study. Uptake rates in house mice were greater than those in voles for both 137Cs and 90Sr. Daily uptake rates in house mice were estimated at 2.72 x 10(12) unstable atoms per gram (whole body) for 137Cs and 4.04 x 10(10) unstable atoms per gram for 90Sr. Comparable rates in voles were 2.26 x 10(11) unstable atoms per gram for 137Cs and 1.94 x 10(10) unstable atoms per gram for 90Sr. By comparing values from voles in the enclosures to those from wild voles caught within 50 m of the enclosures, it was estimated that only 8.5% of 137Cs was incorporated from abiotic sources, leaving 91.5% being incorporated by uptake from biotic materials. The fraction of 90Sr uptake from abiotic sources was at least 66.7% (and was probably much higher). Accumulated whole-body doses during the enclosure periods were estimated as 174 mGy from intramuscular 137Cs and 68 mGy by skeletal 90Sr in house mice over 40 d and 98 mGy from 137Cs and 19 mGy from 90Sr in voles over 30 d. Thus, uptake of radionuclides from abiotic materials in the Red Forest at Chornobyl is an important source of internal contamination.

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Chromosomal distribution of the mys retrotransposon was examined by in situ hy-bridization with a biotinylated probe. Thirty-six mice from four species ofthe Peromyscus leucopus/ maniculatus complex were examined. Mys hybridized to every chromosome in all individuals examined. However, the pattern of hybridization was nonrandom. Mys elements were excluded from C-banding regions of the autosomes, and hybridized preferentially to G-bands. The most prominent feature of these hybridizations was the preferential accumulation of mys on the X and Y chromosomes of all four species examined. Accumulation of mys on the X is incompatible with the hypothesis that selection acting on deleterious mutations is the major mechanism regulating the copy number of this element. Rather, this supports the Langley model for containment of transposable element copy number by unequal exchange during meiosis.

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