Excretion of 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) from rat liver following oral administration of Lactobacillus reuteri and Lactobacillus acidophilus

Oral administration of Lactobacillus reuteri CP3012 or Lactobacillus acidophilus L-92 for 60 days in rats that were previously administered 3,3′,4,4′,5-pentachlorobiphenyl (PCB126) orally at a dose of 100 μg/kg of body weight resulted in a significant decrease in hepatic bioaccumulation of PCB126 (p < 0.05), with levels of 30.7 ± 3.7 ng/g and 92.6 ± 25.0 ng/g of liver tissue, respectively, compared with 133.1 ± 12.7 ng/g of liver tissue in the controls. The electron paramagnetic resonance signal level of the liver PCB126-specific g = 2.49 species in rats administered L. reuteri CP3012 decreased significantly (p < 0.05). Both the bile acid concentration in the feces and total stool output increased significantly following administration of lactobacilli (p < 0.05); however, adsorption of PCB126 onto the bacterial cells was not observed. These results suggest that these bacteria inhibit reabsorption of PCB126 with bile acid by blocking enterohepatic circulation through absorbing and/or deconjugating the bile acids in the intestinal tract and by promoting excretion of bile acids from the body, thus reducing PCB126 accumulation in the liver.