X-Ray-Induced Dominant Lethal Mutations in Mouse Oocytes Detected by an in Vitro Assay

1987 ◽  
Vol 112 (2) ◽  
pp. 374 ◽  
Author(s):  
L. S. Goldstein
2006 ◽  
Vol 3 (3) ◽  
pp. 208 ◽  
Author(s):  
Douglas G. Beak ◽  
Nicholas T. Basta ◽  
Kirk G. Scheckel ◽  
Samuel J. Traina

Environmental Context. Ingestion of soil contaminated with arsenic is an important pathway for human exposure to arsenic. The risk posed by ingestion of arsenic-contaminated soil depends on how much arsenic is dissolved in the gastrointestinal tract. Aluminum oxides are common components in the soil and act as a sink for arsenic. Knowledge of the behavior of arsenic associated with aluminum oxide surfaces in a simulated gastrointestinal tract will provide an understanding of the ingestion risk of arsenic-contaminated soil to humans. Abstract. Arsenate adsorbed to oxide surfaces may influence the risk posed by incidental ingestion of arsenic-contaminated soil. Arsenate sorbed to corundum (α-Al2O3), a model Al oxide, was used to simulate ingested soil that has AsV sorbed to Al oxides. An in vitro assay was used to simulate the gastrointestinal tract and ascertain the bioaccessibility of arsenate bound to corundum. The surface speciation of arsenate was determined using extended X-ray absorption fine structure and X-ray absorption near edge structure spectroscopy. The arsenate sorption maximum was found to be 470 mg kg–1 and the surface speciation of the sorbed arsenate was inner-sphere binuclear bidenate. The AsV was found to only be bioaccessible during the gastric phase of the in vitro assay. When the sorbed AsV was <470 mg kg–1 (i.e., the sorption maxima) the bioaccessible As was below detection levels, but when sorbed AsV was ≥470 mg kg–1 the bioaccessible As ranged from 9 to 16%. These results demonstrate that the bioaccessibility of arsenate is related to the concentration and the arsenate binding capacity of the binding soil.


1960 ◽  
Vol 1 (3) ◽  
pp. 381-392 ◽  
Author(s):  
A. J. Bateman

1. TEM resembles X-rays in inducing dominant lethal mutations in the sperm of rats and mice and sterilizing type B spermatogonia. Beyond this, however, there are several important differences.2. The relative ease with which TEM and X-rays affect sperm and spermatogonia varies greatly. The X-ray dose which produces 50% dominant lethals in sperm (500 rad) sterilizes spermatocytes and type B spermatogonia, and has such a drastic effect on type A spermatogonia that recovery of fertility is delayed for 2½ months. The TEM dose which produces the same mutation rate in sperm (0·1 mg./kg. rat) has no detectable effect on pre-meiotic stages. Even 1 mg./kg. only sterilizes the most sensitive stage, type B spermatogonia.3. Taking immature sperm as the standard, mature sperm are more sensitive to X-rays, but less sensitive to TEM, and early spermatids, the most sensitive stage to X-ray-induced dominant lethals, are highly resistant to TEM.4. Spermatocytes, in which X-rays yield a mutation rate equal to immaturesperm, are highly resistant to TEM.5. To produce the same mutation rate in immature sperm, mice require twice as much TEM as the rat in mg./kg., though approximately the same X-ray dose.6. In contrast to mid-stage rat spermatids, which are the most sensitive stage to TEM, mouse mid-stage spermatids are resistant.


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