No abstract available

No abstract available

[en] Intermittent X radiation administered in 3-R doses for ten successive weeks to RAP mice did not increase the incidence of leukaemia. A total dose of 100 R (10 R weekly) significantly increased the level. A total dose of 300 R (30 R weekly) increased the incidence of leukaemia only slightly but not significantly over that induced by the 100-R total dose. The two leukaemogenic doses of X radiation (100 and 300 R) yielded incidences of leukaemia comparable to those following mean doses of perinatal γ exposure at 200 and 1000 rads. However, continuous lifetime exposure of five successive generations to 30 rads was by far more effective than the higher doses of γ or X radiation. In these wide discrepancies between leukaemogenic effects of equal low doses of γ and X radiation, there are two disparate factors: chronic versus intermittent exposure and the populations at risk - young adult mice versus mice exposed from conception to death. Evidence of a greater sensitivity of immature compared with mature mice is not reflected in the leukaemic incidence or in the projected lifespan of non-leukaemic mice following 1000 rads perinatal γ exposure. Apart from the possible greater effectiveness of chronic exposure, the importance of indirect effects is suggested by the greatly extended lifespan of the 30-R X-irradiated mice as compared with those receiving 30 rads γ. The force of constitutional factors and/or an inhibitory influence of high doses is apparent in the response of rats (NEDH strain) to whole-body single doses within the range 700-1100 R. Single rats, or one of a parabiotic pair thus treated, showed only marginal differences in incidence of leukaemia compared with control rats, and parabiosis alone yielded a comparable incidence of leukaemia. (author)

No abstract available

[en] Spontaneous benign tumors are present in nearly half of NEDH rats. A single whole-body exposure of 1000 R X radiation delivered to a rat supported by a shielded parabiont partner induced high incidence rates of benign tumors in several radioresponsive organs: ovary, 49.7%; adrenal medulla (males, 23.9%; females, 15.2%); mammary tissue (females, 19.6%); islands of Langerhans (males, 15.3%); and liver (cholangiomas) (males, 7.4%; females, 13.8%). Both hormonal imbalance and radiation effects appear to be involved. Parabiosis decreased the incidence of pheochromocytoma, but irradiation of a partner increased it. Mammary tumors occurred on the average 200 days earlier in irradiated rats than in their unirradiated controls. Benign tumors rarely affected health. The incidence was not increased in most organs following irradiation. Three control series were used: single rats, control parabiont rats and the shielded partners of the irradiated partners. Although endometrial polyps were more frequent in irradiated than in shielded partners, they probably resulted from hormonal imbalance. Adenomas of the pituitary were most frequent in shielded female parabiont partners (16.0%). Their incidence was decreased by radiation to 4.2%. Most types of benign tumors rarely progress to malignancy

No abstract available

[en] Leukemia and lymphoid tumors each have a 2 percent spontaneous rate in NEDH rats. Rats are less prone to such tumors than mice. Parabiosis of syngeneic rats permits one partner to survive a whole-body x-ray exposure of 1000 R if the other partner is shielded. Parabiosis alone induced a slight increase in the rates of incidence of both leukemia and solid lymphoid tumors, to about 5 percent. Exposure of one parabiont partner to 1000 R did not increase the incidence rates of these tumors significantly in either partner and sharply decreased the incidence rate of lymphosarcoma in female pairs. Monocytoid and myeloid leukemias were the more common types. Leukemia was often but not always shared by both partners of a pair. The solid lymphoid tumors tended to respond similarly following parabiosis and radiation. These tumors were usually restricted to one partner. Their incidence rates did not differ significantly between the irradiated and shielded partners, for lymphosarcoma 0.3 percent in the irradiated and 1.0 percent in the shielded and for reticulum cell sarcoma 1.1 and 1.5 percent, respectively

No abstract available

[en] Parabiotic pairs of B6.Ly5.1 and B6.Ly5.2 mice were used to investigate how lymphocytes in various organs and various lymphocyte subsets mixed with partner cells. The origin of partner cells was determined by using anti-Ly5.1 mAb in conjunction with immunofluorescence tests. Parabiosis was also produced after the irradiation of B6.Ly5.2 mice at various doses to prepare an immunosuppressive partner. Irrespective of irradiation, lymphocytes and other hematopoietic cells in the bone marrow and lymphocytes in the thymus showed a low mixture of partner cells in comparison with those of all other organs tested. On the other hand, lymphocytes in the blood, spleen, and lymph nodes became a half-and-half mixture of their own cells and partner cell by 14 days after parabiosis. Among lymphocyte subsets, intermediate CD3 cells (i.e., CD3^int cells) and NKT cells (i.e., NK1.1⁺ subset of CD3^int cells) in the liver also showed a low mixture of partner cells. The present results raise the possibility that lymphocytes in the bone marrow and thymus, and extrathymic T cells in the liver might be in situ generated from their own preexisting precursor cells. Another observation was that, after irradiation, partner cells showed accelerated mixture even if they showed a low mixture under non-irradiated conditions. However, only lymphocyte subsets with the same phenotype as those of preexisting cells entered the corresponding sites. (author)

[en] Twelve hundred fifty-two pairs of male NEDH rats were parabiosed, one partner received a single dose of 1000 R x-radiation, and the other rat was shielded with lead. Eleven hundred twenty pairs survived over 200 days and constitute the basis of this report. Twenty-five of the irradiated partners developed malignant tumors of the prostate, 19 of which were adenocarcinomas. One adenocarcinoma appeared in the shielded partners and one in a control group of 586 parabiosed and single rats. The long-term effect of a single dose of 1000 R whole-body x-radiation is weakly carcinogenic for the rat prostate