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ON THE MECHANISM OF ACTION OF X IRRADIATION AND CYTOSTATIC SUBSTANCES ON TUMOR CELLS

Journal Article · · Geburtsh. Frauenheilk.
OSTI ID:4690483

The lethal effects of x rays and cytostatic agents may be attributed to inhibition of glycolysis and protein synthesis as well as to inhibition of DNA synthesis. Inhibition of DNA synthesis may result in deficiency of enzymes involved in cell reproduction; some of the enzymes may be required for DNA synthesis. Either their formation or activation may be blocked by irradiation, whereas direct injury of DNA by radiation may have only a subordinate role in cell death. Synthesis of diphosphopyridine nucleotide (DPN) is also particularly sensitive to radiation, as shown by the finding that irradiated Yoshida ascites sarcoma cells have a lower DPN content after exposure to high doses. However, DNA synthesis is diminished by more moderate doses, in the range of those used in human radiotherapy. The lowered DPN content of irradiated tumor cells may be related to the previously observed postirradiation inhibition of glycolysis and protein synthesis. The cytostatic agent E 39(2,5-bis STAethyleneimino!-3,6- bispropoxy-1,4-benzoquinone) produced parallel changes, inhibiting both DPN synthesis and glycolysis. E 39 could inhibit DNA synthesis under conditions in which glycolysis was unaffected. Treatment of rats with E 39 reduced the incorporation of iron in erythrocytes. It also reduced the half life time of erythrocytes in rats from 14 to 11 to 13 days and in carcinoma patients from 33 to 22 days. (H.H.D.)

Research Organization:
Universitaet, Hamburg-Eppendorf, Ger.
NSA Number:
NSA-17-027035
OSTI ID:
4690483
Journal Information:
Geburtsh. Frauenheilk., Journal Name: Geburtsh. Frauenheilk. Vol. Vol: 23
Country of Publication:
Country unknown/Code not available
Language:
English

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