[en] The radiogenetoxicological effects on the adult testis and the metabolic difference of tritiated thymidine between the testis of young and adult BALB/C mice were studied. When 0.037 MBq/g.b.w. of tritiated thymidine was given i.v. to mice, the initial burden of tritium in the adult was larger than that of tritium in the young. But the retention of tritium in testis of the young gradually become larger than that of tritium in the adult with the passing time. Tritiated thymidine which was incorporated into DNA of the male germ cell nuclei damaged the genetic materials and caused the rising of the rates of the dominant lethal and the dominant mutation which produced skeletal abnomalities in the offspring. The relationship between the dominant lethal mutation index (Y) and the injected activity of tritiated thymidine (I, MBq/g.b.w.) is described by Y = 74.13 + 80.20 I (r = 0.95). The relationship between the incidence of the dominant skeletal mutation in the offspring (B) and the injected activity is B = 0.16 + 0.079 I ( r = 0.85)

[en] Reported effects of some oncogenes, tumour suppressor genes and DNA repair genes on sensitivity of cells to ionizing radiation are reviewed. The role of oncogenes in cellular response to irradiation is discussed, especially the extensively studied oncogenes such as the ras gene family. For tumour suppressor genes, mainly the p53, which is increasingly implicated as a gene affecting radiosensitivity, is reviewed. It is considered that there is a cell cycle checkpoint determinant which is postulated to be able to arrest the irradiated cells in G₁ phase to allow them to repair damage before they undergo DNA synthesis. So far there are six DNA repair genes which have been cloned in mammalian cells, but only one, XRCC1, appears to be involved in repair of human X-ray damage. XRCC1 can correct high sisterchromatid exchange levels when transferred into EM₉ cells, but its expression seems to have no correlation with radiosensitivity of human neck and head tumour cells. Radiosensitivity is an intricate issue which may involve many factors. A scheme of cellular reactions after exposure to irradiation is proposed to indicate a possible sequence of events initiated by ionizing radiation

[en] Doses of enriched uranium in testes inducing dominant lethality and skeletal abnormalities in offsprings are estimated. When intra-testicular injection dose is 0.4∼60 μg enriched uranium; from intake to insemination, testes could receive 9.14 x 10^-5∼1.38 x 10^-2 Gy radiation dose. Experimental results show that with the increase in the absorption dose, the number of living fetuses in a litter decreases, dominant lethality and skeletal abnormalities rise. It should be noted that relationship between the injected dose (I in μg) and the incidence of dominant skeletal abnormalities (S in %) in the offsprings can be represented by equation: S = 28.84 + 0.84I

[en] The purpose of the present study is to ascertain ¹⁴⁷Pm retention in testis and its radiogenotoxicological effects of gene mutation through varying radioactivities of internal exposure. Especially the accumulation of ¹⁴⁷Pm in testis induces the dominant lethal, dominant skeletal mutation and abnormalities in sperm. Studies indicated that the cumulative absorption dose in testis increases as the internal exposure of ¹⁴⁷Pm increases. The internal exposure of ¹⁴⁷Pm can destroy the genetic materials and raise the rates of dominant lethal and dominant mutation of skeletal abnormalities in the offspring. The relationship between the rate of dominant skeletal mutation (B) and accumulated radioactivities of ¹⁴⁷Pm (D) in testis can be described by a linear equation that is B 20.68 + 35.48 D. The relationship between abnormalities of the sperm and the cumulative dose from ¹⁴⁷Pm in testis can be expressed by the following equation: S = 10.8705 D^0.5224 + 3.1768

[en] The metabolic peculiarities of renal radiotracer ^99mTc-PAHIDA and diagnostic use were studied. The results of the radioactive tracing study showed that ^99mTc-PAHIDA was distributed predominantly in kidney, and then in heart, gastrointestinal tract, liver, spleen, musculus quadriceps femoris, adipose tissue, testes and brain. It should be noted that when smaller dose of this agent was given, more ^99mTc-PAHIDA was concentrated in kidney and, at the same time, the level of its binding to plasma protein was lower. The experimental results indicated that ^99mTc-PAHIDA was rapidly excreted in urine. Autoradiochromatographic examination of the urine showed a single radioactive peak corresponding to the authentic ^99mTc-PAHIDA, indicating that ^99mTc-PAHIDA was excreted in the unchanged form. (3 tabs.)

[en] Tracer experiment showed that ^99mTc-PAHIDA was distributed predominantly in kidney. The distribution in other tissue was in the following descending order: heart, gastrointestinal tract, liver, spleen, muscle, adipose tissue, testes, and brain. The smaller the intravenous dose, the lower the proportion of the drug was combined to plasma protein and the more the drug was distributed in kidney. Excretion of ^99mTc-PAHIDa via urine was rapid and was in its original form as shown by radiochromatography

[en] The effectiveness of four chelating agents (Ca-DTPA, Zn-DTPA, quinamic acid and H-73-10) in removing incorporated ²⁴¹Am was studied on 200 rats. The results show that Ca-DTPA and Zn-DTPA are more effective than the others. They decreased the ²⁴¹Am contents in the rat liver and skeleton down to only about 5 and 10 per cent of the control values, respectively. Quinamic acid has the same effectiveness in reducing the ²⁴¹Am contents in the rat skeleton and liver as that of DTPA, but it leads to the cumulation of ²⁴¹Am in the kidney, i. e., the ²⁴¹Am content in the kidney is even higher than that in control rats. Although H-73-10 can remove ²⁴¹Am from the rat organs, it is much less effective than DTPA