The objective of this study was to evaluate the sub-lethal toxicity of hexabromocyclododecane
(HBCDD) in fish. Adult Chinese rare minnows as in vivo models were exposed to waterborne
HBCDD from 1 to 500 microg/l for 14, 28 and 42 days. Hepatic CYP1A1 (ethoxyresorufin-O-deethylase,
EROD) and CYP2B1 (pentaoxyresorufin-O-depentylase, PROD) activities were measured.
At the same time, molecular biomarkers of oxidative stress were also assayed in the
brain, including reactive oxygen species (ROS), lipid peroxidation products (thiobarbituric
acid-reactive substances, TBARS), DNA damage and protein carbonyl, as well as superoxide
dismutase (SOD) activity and glutathione (GSH) content. DNA damage was evaluated using
the Comet assay on erythrocytes. Besides, the content of HBCDD in whole fish was determined
after 42 days exposure. The results show that HBCDD could induce EROD and PROD at
500 microg/l after 28 days exposure, and at 100 to 500 microg/l after 42 days exposure
(P<0.05), respectively. ROS formation in fish brain was observed to be increased in
both time- and dose-dependent manner due to HBCDD exposure. The significant increases
in TBARS and protein carbonyl contents occurred in fish brain after 28 and 42 days
exposure (P<0.05). Significant DNA damage in erythrocytes by Comet assay was also
found in the 100-500 microg/l exposure groups (P<0.05) after 42 days exposure. Moreover,
significant depletion in brain GSH content occurred in all treated groups (P<0.05)
and apparent inhibition in SOD activity in brain was observed in the groups of 10-500
microg/l concentrations during 42 days exposure. The results demonstrate that increasing
duration of HBCDD exposure induced EROD and PROD activities, caused excess ROS formation,
finally resulted in oxidative damage to lipids, proteins and DNA and decreased antioxidant
capacities in fish. Chemical analysis of HBCDD in whole fish showed accumulation up
to 654 microg/g wet weight.