Effects of polychlorinated biphenyls on whole animal energy mobilization and hepatic cellular respiration in rainbow trout, Oncorhynchus mykiss
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- 作者：Rance Nault ; naultran@msu.edu ; Samar Al-Hameedi ; Thomas W. Moon
- 关键词：Polychlorinated biphenyl ; Respiration ; Rainbow trout ; Energetic cost ; Metabolism ; Detoxification
- 刊名：Chemosphere
- 出版年：2012
- 出版时间：May, 2012
- 年：2012
- 卷：87
- 期：9
- 页码：1057-1062
- 全文大小：255 K
文摘
The production of polychlorinated biphenyls (PCBs) was banned in 1977 but these chemicals persist in the environment and threaten aquatic organisms. PCB exposure often results in activation of the aryl hydrocarbon receptor (AhR) and increases in hepatic detoxification mechanisms. Activation of these detoxification mechanisms is believed to be associated with energetic demands that may come at the expense of other physiological processes such as growth, activity and reproduction. We tested the hypothesis that exposure to sub-lethal levels of PCBs results in increased energy demand and energy mobilization using both an in vivo and in vitro approach. Rainbow trout (Oncorhynchus mykiss) received a single intraperitoneal sub-lethal dose (50 ¦Ìg kg?) of 3,3?4,4?5-pentachlorobiphenyl (PCB 126) and left for 10 d after which standard oxygen consumption and plasma and liver metabolites were assessed. PCB 126 exposed trout did not alter standard oxygen consumption but did increase plasma glucose concentration implying the mobilization of glucose to cope with this exposure regime. Cellular respiration was assessed in trout hepatocytes exposed to PCB 126 or PCB 77 (3,3?,4?tetrachlorobiphenyl) two AhR activators but with different potencies (PCB 126 ?#xA0;PCB 77). Mitochondrial respiration was assessed by stimulating complex II with succinate and although no increases in respiration were associated with PCB exposure in non-stimulated cells, PCB 77 impaired mitochondrial respiration by preventing stimulation of complex II respiration and potentially masking any actual energetic costs of PCB exposure. These studies suggest that energy is mobilized upon exposure to PCBs, however, actual increases in energy demand may be overshadowed by impaired mitochondrial respiration.