[en] It has previously been observed that protease inhibitors suppress radiation transformation in vitro. The present study showed that a 24 h treatment with the protease inhibitor antipain at five days post-irradiation was sufficient to significantly suppress radiation transformation. Comparable experiments performed with cycloheximide, an inhibitor of protein synthesis, showed that this metabolic inhibitor could suppress radiation transformation when present immediately following the X-ray exposure but not when present for one day at five days post-irradiation. These results suggest that antipain is suppressing an ongoing cellular process occurring in response to X-irradiation. (author)

[en] It has previously been observed that protease inhibitors suppress radiation transformation in vitro. The present study showed that a 24 h treatment with the protease inhibitor antipain at five days post-irradiation was sufficient to significantly suppress radiation transformation. Comparable experiments performed with cycloheximide, an inhibitor of protein synthesis, showed that this metabolic inhibitor could suppress radiation transformation when present immediately following the X-ray exposure but not when present for one day at five days post-irradiation. These results suggest that antipain is suppressing an ongoing cellular process occurring in response to X-irradiation

[en] The difference in sensitivity to cycloheximide between actively dividing and non-dividing cells was exploited to enhance detection of auxotropic and UV-sensitive mutants in the fungi Schizophyllum commune and Saccharomyces cerevisiae. The antibiotic enrichment technique is used here because it offers the necessary selectivity. The method is of particular importance for selection of UV-sensitive and other conditional mutants in systems that cannot be replica plated

[en] The 32 kDa herbicide binding protein of PSII is degraded rapidly in the light. This phenomenon was investigated in Spirodela oligorrhiza. When fronds were radiolabeled in the presence of cycloheximide only the chloroplast-encoded proteins were labeled. Under these conditions, a breakdown product of 23.5 kDa was observed. This polypeptide was further degraded with kinetics similar to that of the 32 kDa protein. The 23.5 kDa polypeptide cross-reacted with an antibody specific to the 32 kDa protein. By protease digestion it was determined that the 23.5 kDa polypeptide is the intact N-terminal piece of the 32 kDa protein. Thus, this product corresponds to the membrane anchor of the 32 kDa protein. Using the same antibody, breakdown products of 16 kDa, 14 kDa and 12 kDa were observed. These products have also been observed in Zea mays and Solanum nigrum. Using DCMU during pulse-chase experiments at different light intensities, evidence was obtained that the 23.5 kDa breakdown product is generated in vivo

No abstract available

[en] REG (Regenerating gene) Iα protein functions as a growth factor for gastrointestinal cancer cells, and its mRNA expression is strongly associated with a poor prognosis in gastrointestinal cancer patients. We here demonstrated that PPARγ-agonist thiazolidinediones (TZDs) inhibited cell proliferation and REG Iα protein/mRNA expression in gastrointestinal cancer cells. TZDs inhibited the REG Iα gene promoter activity, via its cis-acting element which lacked PPAR response element and could not bind to PPARγ, in PPARγ-expressing gastrointestinal cancer cells. The inhibition was reversed by co-treatment with a specific PPARγ-antagonist GW9662. Although TZDs did not inhibit the REG Iα gene promoter activity in PPARγ-non-expressing cells, PPARγ overexpression in the cells recovered their inhibitory effect. Taken together, TZDs inhibit REG Iα gene transcription through a PPARγ-dependent pathway. The TZD-induced REG Iα mRNA reduction was abolished by cycloheximide, indicating the necessity of novel protein(s) synthesis. TZDs may therefore be a candidate for novel anti-cancer drugs for patients with gastrointestinal cancer expressing both REG Iα and PPARγ.

[en] The radiation sensibility of different fungi was determined and the influence of cycloheximide on radioresistance was tested. The radiation sensitive Byssochlamys fulva and Penicillium terrestre were treated with cycloheximide before γ-irradiation, but no sensitization could be found. The radioresistent Pullularia pullulans, however, pre-treated with 20 μg/ml cycloheximide, showed an increase of the radiation effect; this effect was much lower the organisms were treater after γ-irradiation. (author)

[en] The entry of cells into mitosis was monitored by shaking off mitotic cells from monolayer cultures. The location in G₂ of the x-ray transition point (TP), beyond which the cells were not delayed by x irradiation moved closer to mitosis as the dose was increased, i.e., at 10 min before prophase for 100 to 200 rad, and at 19 min for 30 to 60 rad. Treatment with cycloheximide (CH, 20 μg/ml) at the time of irradiation (50 to 100 rad) shifted the TP for x irradiation by 5 to 9 min toward mitosis. Calculations from these shifts in TP with radiation dose indicated that the logarithm of both the fraction of cells in G₂ not delayed by irradiation and the fraction beyond the TP for CH (located at 26 min before phophase for 5 to 50 μg/ml) not delayed by irradiation decreased linearly with dose (anti D₀ of 30 rad). Furthermore, inhibition of protein synthesis by CH, with or without a simultaneous treatment with actinomycin D (AMD), prevented repair of damage causing mitotic delay for a period of time equal to the duration of the CH treatment

No abstract available

No abstract available