摘要
Perfluorinated organic compounds(PFOCs) are emerging persistent organic pollutants(POPs) widely distributed in the environment,wildlife and human.We studied the toxicology of perfluorooctane sulfonate(PFOS) and perfluorooctanoic acid(PFOA) on immunotoxicity and hepatotoxicity in primarily cultured hepatocytes of freshwater tilapia(Oreochromis niloticus).Cultured hepatocytes were exposed to PFOS or PFOA(0,10,20 and 30 mg/L) for 24,48,72,96,120 and 144 hours,respectively.Oral doses of these compounds that induce significantly detectable immunotoxicity and hepatotoxicity were employed in the study.In response to PFOS,the leukocytes,B cells,granulocytes,and macrophages among the isolation of intrahepatic immune cells(IHIC) from PFOS-treated tilapia produced significant levels of immune cells compared with that of the control group.The numbers of leukocytes,B cells,granulocytes,and macrophages for PFOS-treated tilapia increased with the incremental exposure concentration.Moreover,similar to the findings in PFOA toxicity effects,the erythropoietin levels in tilapia increased with the increase of the PFOS and PFOA concentrations.The lowest doses(10 mg/L) of PFOS exposure led to a marked inhibition in the hepatocyte viability in tilapia.Similarly,tilapia exposed to PFOA demonstrated a similar pattern,and a dose-dependent decrease in the hepatocyte viability was observed in the following treatment of PFOA.In the 72 h exposures,ethoxy-resorufin-O-deethylase(EROD) activity was significantly induced with the increase concentrations in tilapia liver(p<0.05).Tilapia showed a strong EROD induction in livers,and significantly difference in EROD activity was observed between control,PFOS and PFOA-exposed tilapias.The liver glycogen content showed that PFOS and PFOA exposure caused significant changes in the liver glycogen content,which depended on the duration of exposure.And it appeared that the decrease in blood glucose level during the acclimation was followed by significant increase in liver glycogen content in tilapia.
Perfluorinated organic compounds (PFOCs) are emerging persistent organic pollutants (POPs) widely distributed in the environment, wildlife and human. We studied the toxicology of perfluorooctane sulfonate (PFOS) and perfluorooctanoic acid (PFOA) on immunotoxicity and hepatotoxicity in primarily cultured hepatocytes of freshwater tilapia (Oreochromis niloticus). Cultured hepatocytes were exposed to PFOS or PFOA (0, 10, 20 and 30 rag/L) for 24, 48, 72, 96, 120 and 144 hours, respectively. Oral doses of these compounds that induce significantly detectable immunotoxicity and hepatotoxicity were employed in the study. In response to PFOS, the leukocytes, B cells, granulocytes, and macrophages among the isolation of intrahepatic immune ceils (IHIC) from PFOS-treated tilapia produced significant levels of immune cells compared with that of the control group. The numbers of leuko- cytes, B cells, granulocytes, and macrophages for PFOS-treated tilapia increased with the incremental exposure con- centration. Moreover, similar to the findings in PFOA toxicity effects, the erythropoietin levels in tilapia increased with the increase of the PFOS and PFOA concentrations. The lowest doses (10 mg/L) of PFOS exposure led to a marked inhibition in the hepatocyte viability in tilapia. Similarly, tilapia exposed to PFOA demonstrated a similar pattern, and a dose-dependent decrease in the hepatocyte viability was observed in the following treatment of PFOA. In the 72 h exposures, ethoxy-resorufin-O-deethylase (EROD) activity was significantly induced with the increase concentrations in tilapia liver (p〈0.05). Tilapia showed a strong EROD induction in livers, and significantly differ- ence in EROD activity was observed between control, PFOS and PFOA-exposed tilapias. The liver glycogen content showed that PFOS and PFOA exposure caused significant changes in the liver glycogen content, which depended on the duration of exposure. And it appeared that the decrease in blood glucose level during the acclimation was fol- lowed by significant increase in liver glycogen content in tilapia.
基金
supported by Chongqing Key Laboratory of Micro/Nano Materials Engineering and Technology (No. KFJJ1106)
Jiangsu Provincial Key Laboratory of Coastal Wetland Bioresources and Environmental Protection (No.JLCBE11004)
Jiangsu Marine Resources Development Research Institute (No. JSIMR10E04)