Distribution and mechanism of uptake of 111InCl3 in a tumor model for lymph node metastases

Abstract

The localization of ¹¹¹In activity in the tumor and draining lymph nodes of the H-4-II-E ACI rat hepatoma was investigated following the injection of ¹¹¹In-chloride. In this tumor model, the tumors metastasize to the regional lymph nodes in male rats only. The following experiments were performed: (a) biodistribution of ¹¹¹In; (b) correlation of ¹¹¹In uptake with [³H]thymidine; (c) γ camera imaging; (d) autoradiography; (e) iron competition and (f) binding of ¹³¹I-transferrin to H-4-II-E cells. Tumor-to-muscle ratios of ¹¹¹In in males were 4.9:1 in the primary tumor and 9.1:1 in the metastatic lymph nodes 24h post injection. In the lymph node metastases in the males, a significant correlation between ¹¹¹In uptake and [³H]thymidine was observed (r = 0.737) suggesting that ¹¹¹In uptake in the metastases is related to cellular proliferation. No such correlation was observed in either primary tumors (both male and female) or in the draining lymph nodes of the females. Metastatic lymph nodes in males could be detected in γ camera images while draining nodes in females could not be delineated. Injection of ferric citrate prior to ¹¹¹In administration resulted in a significant reduction of ¹¹¹In uptake in the liver, spleen and tumor and increased the amount of activity recovered from the kidney. Measurements of the binding of ¹³¹I-labeled rat transferrin to H-4-II-E cells in vitro suggest that these cells display transferrin receptors.