| Background and objectives: 2,3,7,8-tetrachlorinated-dibenzo-p-dioxin (TCDD) is one of the prototypical persistent organic pollutants and has been shown to potentially impair the cognitive functions at higher doses with prenatal, postnatal, lactational, or acute exposure. However, there is little confirmed information on its effects at very low doses with long term exposure on learning and memory ability and synaptic plasticity in the hippocampus in adult animals. The present study was designed to do so.Materials and methods: 120 one-month-old SD rats were allocated randomly into 4 groups with 30 rats in each group (male: female =1:1). Animals were treated daily with three does of TCDD (i.e. 2 ng/kg/day, 10 ng/kg/day, 50 ng/kg/day), and one control of corn oil. 13 weeks later, all rats were tested using Morris Water Maze (MWM) and the long term potentiation (LTP) in hippocampus CA1 region was recorded lively. Animal's hippocampus and serum were used to observe their morphology of hippocampus and measure the thyroid hormones. Data were analyzed by one-way ANOVA, covariate ANOVA, multivariate ANOVAs, repeated measures ANOVAs, Chi-square tests, correlation analysis and nonparametric test where appropriate. P≤0.05 was regarded as statistical significance.Results:1. No serious visible toxicity was found in TCDD treated rats regarding to activity, the food and water consumption. Subchronic TCDD exposure did not interfere rats'body weight.2. MWM: In female rats: no obvious differences were found in the navigation trial and spatial probe between TCDD treatment groups and controls. In male rats: there were no statistical significance in the eacape latency, times of crossing the former platform, time stayed in the target quadrant, swimming speed and percent distances in the target quadrant. The searching strategy showed statistical significance among all groups (χ2 = 13.29, P<0.05).3. TCDD treatment showed significant effects on LTP: the LTP amplitude and slope were significantly reduced in 2 ng/kg/day; while it was not maintained in the two higher TCDD doses considering the fEPSP induced by HFS. Average amplitude and slope after HFS exhibited a dose-dependent reduction in TCDD-treated animals and were negatively related to the amount of TCDD. 4. Under light microscope, the pyramidal cells'distribution in hippocampus of TCDD treated rats showed sparser than control, however, no statistical significance in any index was found in the stereology analysis. The ultrastructural observation found some damages in the pyramidal cells of TCDD treated groups, mainly, the mitochondrial vacuole, and endoplasmic reticulum in concentric circles.5. The serum thyroid hormone, in the female rats: the concentration of FT3 was the lowest in the group of 2 ng/kg/day (3.97±0.80 p mol/L); the concentration of FT4 was the lowest in the groups of 50 ng/kg/day (8.94±2.38 p mol/L); there was no significance in TT3 among groups. In the male rats: there was no significance in FT3 among groups; the concentration of FT4 was the highest in the group of 2 ng/kg/day (15.05±3.30 p mol/L); the concentration of TT3 was the highest in the group of 50 ng/kg/day (0.55±0.07μg/L). There were no significant differences in the gender and groups in the concentration of TT4. There was no statistical significance in TSH in gender, but statistical significance among groups (χ2=11.59, P<0.05).Conclusions: Subchronic TCDD exposure may have trivial effects on the spatial learning and memory ability in adult rats, but it does damage the neural synaptic function in the CA1 region of hippocampus. TCDD may damage the mitochondria of pyramidal cells. The homeostasis of thyroid hormone may be disrupted. This study indicates the potential harm of dioxin at low level on cognition ability in common population. |
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