Distribution and mechanism of uptake of 111InCl3 in a tumor model for lymph node metastases.
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) gamma 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 24 h 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 gamma 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.