|
Objective: benzo [a] pyrene (benzo (a) pyrene, B (a) P) as the representative of PAHs, widely present in various environmental media, with strong carcinogenic. PCBs are extremely concerned about the current international A class of persistent organic pollutants, polychlorinated biphenyls 126 (3,3 ', 4,4' ,5-pentachlorobipheny, PCB126) as having coplanar polychlorinated Union benzene homologues representatives, one of the most toxic PCBs in the environment and the human body can be detected. Studies have shown that B (a) P metabolic activation can cause cellular oxidative stress, and PCBs can enhance B (a) P metabolic activation, which may aggravate the degree of oxidative stress, thereby causing cell genetic damage, and both often coexist in a variety of environmental media and human biological samples, the researchers combined effects of both oxidative stress and genotoxic effects of practical significance. Methods: in HepG2 cells as target cells, located 0.01,0.1,1 and 10nmol / L PCB126 dose group and B (a) P 50μmol / L dose to 10 ml / L dimethylsulfoxide (DMSO) as solvent control group, for each individual substance exposure. PCB126 also pretreated with different concentrations of HepG2 cells, and then with B (a) P combined exposure. By flow cytometry of intracellular reactive oxygen species (reactive oxygen species, ROS) levels; through TNB assay intracellular glutathione (reduced glutathione, GSH) content; through thiobarbituric acid assay of intracellular malonyl aldehydes (malondialdehyde, MDA) content; and through the single cell gel electrophoresis assay to detect DNA damage, in order to investigate the PCB126 on B (a) P induced oxidative stress in HepG2 cells and genetic damage effects. Results: Compared with the solvent control, PCB126 exposure alone, only at the highest concentration (10.0nmol / L) induced ROS increase (P lt; 0.05). And B (a) P alone compared, PCB126 each dose with 50μmol/LB (a) P joint exposure, ROS were significantly increased (P lt; 0.01), which 0.01,0.10,1.00 nmol / L PCB126 and B ( a) P when the joint exposure induced a dose dependent increase in ROS, ROS increase in 10.0nmol / L PCB126 and B (a) P joint exposure time declined. Compared with the solvent control, 50μmol/LB (a) P alone can cause HepG2 cells exposed to GSH significantly increased (P lt; 0.01), while the exposure time of each dose PCB126 alone GSH were significantly reduced (P lt; 0.01). And B (a) P alone compared to the combined effects of GSH were significantly reduced (P lt; 0.01). Compared with the solvent control, 50μmol/LB (a) P exposure alone can cause a significant increase in HepG2 cell line MDA (P lt; 0. 01). And B (a) P alone compared to only in the highest concentration 10.0nmol / L PCB126 and B (a) P joint exposure of MDA increased significantly (P lt; 0.05). Compared with the solvent control, 50μmol/LB (a) P exposure alone can cause DNA damage was significantly higher (P lt; 0.01). And B (a) P alone compared, 1.00,10.0 nmol / L PCB126 and B (a) P joint exposure significantly increased when DNA damage (P lt; 0.05). Conclusion: In summary, a certain dose of PCB126 make B (a) P-induced oxidative stress increased in HepG2 cells enhanced genetic damage, suggesting that PCB126 on B (a) P may be related to enhanced genotoxicity induced oxidative stress about.
|