Liu Li, Chen Han-yi, Yao Guo-ying, Zhang Hao, Zheng Wei-wei, Wei Xiao, Chen Xin, Jiang Song-hui, Qu Wei-dong
Key Laboratory of Public Health and Safety, Ministry of Education, Department of Environmental Health, School of Public Health, Fudan University, Shanghai, China.
Zhonghua Yu Fang Yi Xue Za Zhi. 2010 Apr;44(4):334-8.
To assess thyroid disruption induced by sodium pentachlorophenol (PCP) using Organization for Economic Co-operation and Development (OECD) recommended TG 407 method.
A total of 30 specific pathogen free (SPF) SD adult male and female rats were randomly divided into 3 groups, and treated with water, 0.33 and 30 mg x kg(-1)x d(-1) of PCP-Na by oral gavage for consecutive 28 days, respectively. After final treatment, histological changes of thyroid were observed by hematoxylin-eosin stain, and the levels of thyroid hormones (total thyroxine (TT(4)), free thyroxine (FT(4)), total triiodothyronine (TT(3)), and free triiodothyronine (FT(3))) were determined by radioimmunoassay. The expression levels of thyroid receptors (TRalpha and TRbeta) mRNA and deiodinases (DioI, DioII and DioIII) mRNA in liver were analyzed by RT-PCR.
In high dose group, liver weight coefficient of male and female rats were (4.82 +/- 0.42)% and (4.99 +/- 0.17)%, increased by 36.2% (t = 7.338, P < 0.01) and 41.8% (t = 8.955, P < 0.01), compared to control group ((3.54 +/- 0.14)%, (3.52 +/- 0.19)%), respectively, while the significant changes of kidney or thyroid weight were not observed. In high dose group, the levels of TT(4) and FT(4) in serum of male rats were (64.95 +/- 7.16) nmol/L and (8.16 +/- 2.29) pmol/L, and decreased by 26.6% (t = -3.999, P < 0.01) and 42.3% (t = -4.112, P < 0.01) compared to control group ((88.48 +/- 6.99) nmol/L, (14.13 +/- 1.68) pmol/L). In the same group, FT(4) in serum of female rats was (4.94 +/- 0.89) pmol/L, decreased by 55.5% (t = -3.380, P = 0.012) compared to control group ((11.10 +/- 3.40) pmol/L) and TT(3) and FT(3) in serum of female rats were (1.92 +/- 0.24) nmol/L and (3.05 +/- 0.79) pmol/L, increased by 74.5% (t = 5.263, P < 0.01) and 55.6% (t = 3.495, P < 0.01) compared to control group ((1.10 +/- 0.23) nmol/L, (1.96 +/- 0.32) pmol/L), respectively. PCP-Na didn't affect the expression levels of TRalpha, TRbeta, DioIII mRNA in high dose group, while DioII expression of male rats (0.209 +/- 0.017) down-regulated by 79.2% (t = -5.426, P < 0.01) compared to control group (1.006 +/- 0.137), and DioI expression of female rats (1.844 +/- 0.189) up-regulated by 66.6% (t = 4.359, P < 0.01) compared to control group (1.005 +/- 0.083), indicating DioI and DioII poss different sensitivity to adverse effects induced by PCP-Na between male and female rats. The histopathological results showed that PCP-Na could give rise to hyperplasia of the follicular epithelium cells, and the depletion of colloid. There were no significant changes in serum THs levels and expression of TRalpha, TRbeta, DioI-IIImRNA in low dose group. However, sporadic lymphocytic infiltration, follicles amplification in part and slightly increased in thickness of follicular cells were observed in this group.
PCP is a kind of thyroid disrupting chemical.
采用经济合作与发展组织（OECD）推荐的TG 407方法评估五氯酚钠（PCP）对甲状腺的干扰作用。
将30只无特定病原体（SPF）的SD成年雌雄大鼠随机分为3组，分别给予水、0.33和30 mg·kg⁻¹·d⁻¹的PCP-Na灌胃，连续28天。末次处理后，采用苏木精-伊红染色观察甲状腺组织学变化，放射免疫法测定甲状腺激素（总甲状腺素（TT₄）、游离甲状腺素（FT₄）、总三碘甲状腺原氨酸（TT₃）和游离三碘甲状腺原氨酸（FT₃））水平。采用RT-PCR分析肝脏中甲状腺受体（TRα和TRβ）mRNA和脱碘酶（DioI、DioII和DioIII）mRNA的表达水平。
高剂量组雄性和雌性大鼠肝脏重量系数分别为（4.82±0.42）%和（4.99±0.17）%，与对照组（（3.54±0.14）%，（3.52±0.19）%）相比分别增加36.2%（t = 7.338，P < 0.01）和41.8%（t = 8.955，P < 0.01），而肾脏或甲状腺重量未见明显变化。高剂量组雄性大鼠血清中TT₄和FT₄水平分别为（64.95±7.16）nmol/L和（8.16±2.29）pmol/L，与对照组（（88.48±6.99）nmol/L，（14.13±1.68）pmol/L）相比分别降低26.6%（t = -3.999，P < 0.01）和42.3%（t = -4.112，P < 0.01）。同组雌性大鼠血清中FT₄为（4.94±0.89）pmol/L，与对照组（（11.10±3.40）pmol/L）相比降低55.5%（t = -3.380，P = 0.012），雌性大鼠血清中TT₃和FT₃分别为（1.92±0.24）nmol/L和（3.05±0.79）pmol/L，与对照组（（1.10±0.23）nmol/L，（1.96±0.32）pmol/L）相比分别增加74.5%（t = 5.263，P < 0.01）和55.6%（t = 3.495，P < 0.01）。高剂量组PCP-Na对TRα、TRβ、DioIII mRNA表达水平无影响，而雄性大鼠DioII表达（0.209±0.017）与对照组（1.006±0.137）相比下调79.2%（t = -5.426，P < 0.01），雌性大鼠DioI表达（1.844±0.189）与对照组（1.005±0.083）相比上调66.6%（t = 4.359，P < 0.01），表明DioI和DioII对PCP-Na诱导的雌雄大鼠不良反应敏感性不同。组织病理学结果显示，PCP-Na可引起滤泡上皮细胞增生和胶体减少。低剂量组血清甲状腺激素水平及TRα、TRβ、DioI-IIImRNA表达无明显变化。然而，该组可见散在淋巴细胞浸润、部分滤泡扩大及滤泡细胞厚度略有增加。
PCP是一种甲状腺干扰化学物。
