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Influence of Transitory, as Compared with Permanent, High-Altitude Exposure on the Pathogenesis of Spontaneous and X-ray-induced Neoplasms in RF/Un Mice¹

Laboratorio de Oncologia, Instituto de Investigaciones de la Altura, Universidad Peruana Cayetano Heredia, Lima, [P. M. C., M. S. J.], Peru and Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tennessee 37830 [A. C. U., J. W. C.]

This study was undertaken to investigate the mechanisms of effects of high altitude on spontaneous and irradiation-induced neoplasia, with particular reference to the influence of the time and duration of high-altitude exposure on the pathogenesis of such growths. Female RF/Un mice exposed to 150 R whole-body X- or sham irradiation at 10 weeks of age were subsequently housed at high (4540 m) or low (150 m) altitude for various lengths of time. In such animals, the overall incidence of neoplasms was increased and the life-span was decreased by irradiation, irrespective of altitude; animals residing at high altitude into old age showed further life shortening with a decrease in the overall incidence of neoplasms, in addition to polycythemia, impairment of weight gain, lymphoid atrophy, decrease in the incidence of lymphoreticular tumors, and increase in the incidence of pulmonary neoplasms, angiomatoid, telangiectatic, and thrombotic lesions, myocarditis, and pneumonia. In animals residing at high altitude for only 3 months after irradiation, the effects of high altitude were drastically reduced; however, the induction of granulocytic leukemia in such animals was enhanced, perhaps through hypoxiainduced stimulation of hemopoietic stem cells which had not yet recovered from irradiation. Since the long-term effects of high-altitude exposure prolonged into old age were not reproduced by transitory exposure early in adult life, the effects may have been mediated largely through influences on late stages in the pathogensis of neoplasms and other age-related lesions, as opposed to early stages in their development.

¹ This research was sponsored by the National Cancer Institute-Atomic Energy Commission Carcinogenesis Program, Biology Division, Oak Ridge National Laboratory, Oak Ridge, Tenn., and was supported in part by Research Grant R01 CA 08264 from the National Cancer Institute, NIH, USPHS.

² Present address: Health Sciences Center, State University of New York at Stony Brook, Stony Brook, N. Y. 11790.

Received 4/ 9/73. Accepted 10/26/73.