Studies On The Toxicity Impact Of Decabrominated Diphenyl Ether In Mice

BDE-209 is the most important flame retardant. Human exposure to BDE-209 has largely forcused on the dietary pathway. At present, studies on the toxicity of BDE-209 are mainly focused on the effects of the adult animals after the neonatal exposure to BDE-209, or the effects of the offspring after the mother exposure. However, little is known about the possible direct neurotoxic effects of BDE-209 on the experimental animals themselves. In this paper, we study the toxicological impact of BDE-209 on mice and explore the mechanism preliminarily.Adult CD-1 Swiss mice (1 0 weeks old) were used for the experiment. All mice were weighed 24±2 g at time of treatment. After a 5-day acclimatisation period, the healthy mice were randomly divided into five groups. Mice of each group were administrated by gastro-gavage with 0, 0.1, 40, 80, 160 mg/kg BDE-209. The exposure time was 15, 30 and 60 days, respectively. After the 60 days exposure, the mice were feed in normal ways for 20, 40 and 60 days in order to observe the effect of self repair. The activities of XOD, GOT and GPT in serum were determined to estimate the effect of BDE-209 on liver. And the activities of TchE, SOD and MDA in brain were determined to explore the neurotoxicity of BDE-209 in mice. The self-repair of brain was also explored.The results were as follows:1. Body weights of the female were inhibited obviously (P<0.05) by BDE-209, compared with the control group. No significant difference was found in male groups.2. The organ index had no significant changes in all infected groups, compared to the control group. And the morphology of liver and spleen has changed in infected groups compared with the control group.3. A significant increase (P<0.05) appeared in the activities of XOD after exposure to BDE-209 15 days except the group of the 0.1 mg/kg level. Then with the increase of exposure time and dose, the activities of XOD increased slightly. And a significant increase (P<0.05) was found in the activities of GOT and GPT after exposure to BDE-209 different time in the 160 mg/kg group. And there was a significant increase (P<0.05) in the 80 mg/kg group after exposure BDE-209 for 60 days.4. The activity of TchE increased at first and with the increase of exposure time and dose, the activities in all infected groups decreased slightly compared with the control group. SOD activities were decreased obviously (P<0.05), and the activities of MDA increased (P<0.05) in all infected groups compared with the control group after exposure to BDE-209 for the designed time except 0.1 mg/kg group.In summary, the organ index was not affected by BDE-209. But the morphology of liver, spleen and brain has changed in infected groups compared with the control group. BDE-209 can induce damage on liver and nervous system in mice. The two possible mechanisms of BDE-209 neurotoxicity were suggested. (1) affecting the production and release of the neurotransmitters through changing the TchE activity (2) inducing the neurotoxicity through the lipid peroxidation.