To investigate the red blood cell destruction that seems to be one cause of anemia accompanying malignant tumors, we examined the enhanced destruction of heat-damaged red blood cells, and the transaction and excretory function to urine of the destroyed cells. Rats with experimentally-induced oral carcinomas were injected with
51Cr-labeled heat-damaged red blood cells. The disappearance of
51Cr from the blood cells, the uptake of
51Cr in the rats' reticuloendothelial system, especially their spleens and in tumor tissues, and excretion of
51Cr in the rats' urine, were examined over time. Their spleens and tumor tissues were observed histopathologically.
Compared with controls, rats with carcinoma showed the following results. The time for disappear-ance of
51Cr from the blood cells, and the time for excretion of
51 Cr in urine, were both prolonged. Although the uptake of
51Cr decreased in the liver, spleen, and bone marrow, it increased in the tumor tissues. In the spleen, there was a decrease in the number of macrophages phagocytizing hemosiderin at the marginal sinus and red pulp. There was increased deposition of hemosiderin in the stroma, and in some cancer pearls of the tumor tissues.
These results suggest that there is a decrease in the destruction of red blood cells in the spleen and excretion of
51Cr to urine, and bleeding is seen in tumor tissue in rats with oral carcinomas.
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