[en] Lipiodol has important diagnostic and therapeutic uses in hepatoma. However, the mechanisms of its selective, prolonged retention in hepatoma cells is not well understood. Therefore, using oil-red O, light and electron microscopy and neutron activation analysis we have determined that HepG2 cells are characterized by lipiodol deposition and emulsification on the cell surface, action uptake of lipodol by endocytosis, and prolonged intracellular retention. These findings may have major clinical significance in the development of a new treatment for hepatoma patients

[en] In our research, a radioactive boron compound, B-I-131-lipiodol, that can be selectively retained in hepatoma cells was prepared. Combining the effect of α particles produced by boron neutron capture reaction with the β particles released by radionuclides in the radioactive boron compounds will produce a synergistic killing effect on cancer cells. Human hepatoma HepG2 cell cultures were used to examine the stability and the intracellular distribution of the radioactive boron drug. Microscopes were used to examine the interaction and retention of B-I-131-lipiodol globules in the individual hepatoma cell. Moreover, ICP-AES and NaI scintillation counter were performed to determine boron concentrations and I-131 radioactivity, respectively. Results showed that B-I-131-lipiodol with a boron concentration and a specific radioactivity ranged from 500-2000 ppm and 0.05-10 mCi/mL respectively was stably retained in serum. The radiochemical purity of B-I-131-lipiodol was 98%. After supplement with a medium containing B-I-131-lipiodol, the HepG2 cells had intracellular B-I-131-lipiodol globules in the cytoplasm as seen by inverted light microscope, the I-131 and boron can be stably retained in HepG2 cells. (author)

[en] The distribution of Lipiodol in the liver and lungs following arterial or portal injection was studied in normal (n=55) and cirrhotic rats (n=20). Using magnified xeroradiography and radioisotope labeled tracers, it was found that Lipiodol was deposited mainly in the liver and lung after either arterial or portal administration. In control rats after arterial injection, deposits in the lung peaked after 2 hours and gradually declined over 48 hours; whereas after portal injection, the deposit steadily increased for 48 hours. Twenty-five percent of cirrhotic rats demonstrated a Lipiodol-induced miliary pattern in the lung. An increased number of portosystemic shunts in cirrhotic rats was also noted. These results suggest that cirrhosis of the liver may be a potential risk factor for developing pulmonary complications after Lipiodol administration. (orig.)

[en] This study attempted to increase BNCT efficiency for hepatoma by a combined treatment of phenylboric acid derivative entrapped lipiodol nanoparticles (PBAD-L nanoparticles) with boric acid. The size of PBAD-L nanoparticles were 400-750 nm at the boron concentrations of 0.3-2.7 mg/ml. After 24 hours the boron concentration in PBAD-L nanoparticles treated human hepatoma HepG2 cells was 112 ppm, while that in rat liver Clone 9 cells was 52 ppm. With the use of 25 μg B/ml boric acid, after 6 hours the boron concentration in HepG2 and Clone 9 cells were 75 ppm and 40 ppm, respectively. In a combined treatment, boron concentration in HepG2 cells which were treated with PBAD-L nanoparticles for 18 hours and then combined with boric acid for 6 hours was 158 ppm. After neutron irradiation, the surviving fraction of HepG2 cells treated with PBAD-L nanoparticles was 12.6%, while that in the ones with a combined treatment was 1.3%. In conclusion, the combined treatment provided a higher boron concentration in HepG2 cells than treatments with either PBAD-L nanoparticles or boric acid, resulting in a higher therapeutic efficacy of BNCT in hepatoma cells. (author)

[en] Hepatocellular carcinoma remains widely prevalent in tropical Africa and south-east Asia. At present, there are no effective treatments for hepatoma and its prognosis is extremely poor unless the tumor was diagnosed in an early stage and resected before metastasis. Therefore, boron neutron capture therapy (BNCT) may provide an alternative therapy for treatment of hepatocellular carcinoma. In this study, the intracellular concentrations of L-boronophenylalanine (BPA), sodium borocaptate (BSH) and boric acid (BA) were examined in human hepatoma HepG2 and liver Clone 9 cell cultures. With the use of 25 μg B/mL media of BPA, BSH and BA, the intracellular uptake of boron in HepG2 and Clone 9 cells was compared. The suitability of BPA, BSH and BA were further evaluated on the basis of organ-specific boron distribution in normal rat tissues. BPA, BSH and BA were administered via intraperitoneal injection into rats with corresponding boron concentrations of 7, 25, and 25 mg/kg body weight, respectively. The accumulation rates of BPA, BSH and BA in HepG2 cells were higher than that of Clone 9 cells. Boron concentration in BPA, BSH and BA treated HepG2 cells were 1.8, 1.5, and 1.6-fold of Clone 9 cells at 4 h, respectively. In both HepG2 and Clone 9 cells, although the concentration of boron in BPA-treated cells exceeded that in BA-treated ones, however, cells treated with BPA had similar surviving fraction as those treated with BA after neutron irradiation. The accumulation ratios of boron in liver, pancreas and kidney to boron in blood were 0.83, 4.16 and 2.47, respectively, in BPA treated rats, and 0.75, 0.35 and 2.89, respectively, in BSH treated rats at 3 h after treatment. However, boron does not appear to accumulate specifically in soft tissues in BA treated rats. For in situ BNCT of hepatoma, normal organs with high boron concentration and adjacent to liver may be damaged in neutron irradiation. BPA showed high retention in pancreas and may not be a good drug for BNCT of hepatoma. BSH had higher retention in liver but low level in pancreas and spleen appears to be a better candidate BNCT drug for hepatoma. These preliminary results provide useful information on future application of BNCT for hepatoma.