Abstract
Toxic oil that caused the disease called Kanemi “Yusho” contained polychlorobiphenyl (K-PCB) and polychlorodibenzofuran (K-PCDF). K-PCB and K-PCDF were separated from the toxic oil, and administered to two groups of mice orally. K-PCB (15.4μg/mouse/day) or a mixture of K-PCB and K-PCDF (15.4μg+1.0μg/mouse/day) was administered every day for 7 consecutive days. In both groups the concentration and biological half-life (B. H. L.) of each PCB isomer were estimated in the liver and adipose tissue.
The PCB isomers containing 4--7-chlorinated compounds showed the highest concentrations in the liver in both groups 1 day after the last oral administration. In the adipose tissue of both groups, 4- and 5-chlorinated PCBs exhibited the highest concentration on day 1, and 6- and 7-chlorinated PCBs on day 10.
The CB% of each PCB isomer (the concentration of each PCB isomer relative to that of the total PCB isomers as a percentage) was examined on day 1 in the K-PCB group. In both liver and adipose tissue, the total CB% of 4- and 5-chlorinated PCBs containing 2, 4-3′, 4′-tetrachlorobiphenyl (peak 9), 3, 4-2′, 4′, 5′-pentachlorobiphenyl (peak 25) and 3, 4-2′, 3′, 4′-pentachlorobiphenyl (peak 28) as the main components was 66.2% in adipose tissue and 57.3% in the liver. On day 50, however, the total CB% of 6- and 7-chlorinated PCBs containing 2, 4, 5-2′, 4′, 5′-hexachlorobiphenyl (peak 29), 2, 3, 4-2′, 4′, 5′-hexachlorobiphenyl (peak 32), 3, 4-2′, 3′, 4′, 5′-hexachlorobiphenyl (peak 47) and 2, 4, 5-2′, 3′, 4′, 5′-heptachlorobiphenyl (peak 49) as the main components was 89.6% in adipose tissue and 86.8% in the liver. A similar tendency was seen in the K-PCB+K-PCDF group. Moreover, in both groups the residual amount of PCBs unsubstituted with chlorine atoms in the meta and para positions (3, 4; 4, 5; 3′, 4′; 4′, 5′) with respect to the biphenyl bridge was small.
B. H. L. of each PCB isomer ranged from 1.92 days at peak 9 to 40.85 days at peak 47 in adipose tissue and from 1.64 days at peak 9 to 21, 71 days at peak 29 in the liver. In general, B. H. L. was shorter in the liver than in adipose tissue. When mice were administered with K-PCB plus K-PCDF, B. H. L.'s at peaks 9, 25 and 28 in liver and adipose tissue were reduced markedly to about one-half of those in mice administered with K-PCB alone. K-PCDF had little effect upon the B. H. L. of the total PCB.
