One-cell mouse embryos of the Balb/c strain normally divide at 18.5 h p.c. (post conception), but they suffer an extremely long G2 arrest when irradiated with 2 Gy X-rays 8 h p.c. at the early pronuclear stage. This could be an indirect effect of radiation on tyrosine dephosphorylation of the p34cdc2 subunit of a maturation or mitosis promoting factor (MPF), which normally occurs at the end of G2. This, in turn, would maintain MPF in an inactivated form and block entry into mitosis. Preliminary studies were undertaken at the morphological level to assess indirectly the validity of this hypothesis. For this purpose, irradiated and control embryos were exposed to different compounds, which are known to interfere, directly or indirectly, with the state of phosphorylation/dephosphorylation of p34cdc2. Caffeine (CAF; 2 mM) did not affect the time of first division of control embryos, but it completely suppressed the radiation-induced G2 arrest of embryos exposed to this compound from 17 h p.c., i.e. 1.5 h before the normal time of first cleavage. Under the same conditions, okadaic acid (OA; 3 microM), a specific inhibitor of phosphatases I and IIA, induced a rapid pronuclear membrane breakdown and a block of all control and irradiated embryos at metaphase. Genistein (GEN; 92 or 185 microM). A potent inhibitor of tyrosine kinases, increased the radiation-induced G2 arrest and even induced a dose-dependent G2 arrest in the control embryos. Embryos were exposed at different times following irradiation to a mixture of either CAF (2 or 5 mM) or OA (3 or 10 microM), and cycloheximide (CH; 5 micrograms/ml), a potent protein synthesis inhibitor. Reversion of G2-arrest by CAF was still seen in embryos exposed to CAF+CH from 17 h p.c. However, the proportion of irradiated embryos eventually able to cleave was lower than that obtained under the conditions of exposure to CAF alone. Embryos exposed to CAF+CH before 17 h p.c. were not able to cleave, regardless of the concentration of CAF used. Nuclear envelope breakdown still occurred in 100% control and irradiated embryos, following exposure to 3 microM OA+CH from 10 h p.c., or to 10 microM OA+CH from 8.5 p.c.(ABSTRACT TRUNCATED AT 400 WORDS)
Methods for collecting and processing blood samples are critical in determining reliable circulating TGFbeta1 levels. Increased TGFbeta1 plasma levels observed in patients with lung cancer are related, at least partly, to concomitant NMPD and also to platelet degranulation as proved by increased betaTG levels.
The study aimed to investigate whether the determination of chromosome aberrations in circulating blood lymphocytes could be useful to assess whole-body exposure from radioactive iodine released accidentally. Ten patients treated with two doses of 1850 MBq of 131I given 24 h apart for thyroid cancer were studied for chromosome aberrations (dicentrics) in blood samples taken before and at various times after exposure. The increase in the yield of aberrations caused by the exposure to iodine was small but statistically significant. Compared to published values for whole-body doses after such treatment, this increase appears to be somewhat smaller than expected from dose-effect relationships obtained for an acute exposure of lymphocytes in vitro or in vivo, a fact which could be explained by the low dose rate of the 131I exposure. Thus, in situations where a population was exposed as a result of the release of radioactive iodine, a determination of chromosome aberrations in blood lymphocytes would not appear to be very useful to determine exposure from iodine.
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