School of Public Health, Seoul National University, Seoul, Korea.
Environ Toxicol Chem. 2011 Apr;30(4):870-7. doi: 10.1002/etc.443. Epub 2011 Feb 8.
Exposure to perfluorooctane sulfonic acid (PFOS) is known to induce thyroid-related adverse effects in aquatic organisms. Because an antioxidant defense mechanism is one of the key functions of the thyroid gland, we examined whether preexposure to PFOS could disrupt thyroid function and enhance cadmium (Cd)-induced oxidative stress in fish. Zebrafish embryos were exposed to control or 0.5 mg/L PFOS for 7 d after fertilization and subsequently exposed to 0.038 mg/L of Cd(2+) or a mixture of the PFOS and Cd for an additional 3 d until 10 d postfertilization (dpf). Survival rates, body length, messenger RNA (mRNA) expressions related to thyroid function and oxidative stress, the levels of thyroid hormones, and malondialdehyde and antioxidant enzyme activities were measured. Significant down-regulation of mRNAs related to thyroid function (thyroid hormone receptor-alpha [THRα], thyroid hormone receptor-beta [THRβ], hematopoietically expressed homeobox [hhex], and paired box gene 8 [pax8]) and decrease of throxine (T4) levels were observed in the PFOS preexposure group, suggesting that PFOS preexposure would influence the performance of thyroid gland in the later stages of life. Certain genes relative to oxidative stress, such as superoxide dismutase 1 (sod1) and heat shock protein 70 (hsp70), in the PFOS preexposure group were significantly up-regulated when the larvae were subsequently exposed to Cd or to the mixture of PFOS and Cd. Glutathione S-transferase activity and malondialdehyde levels of the PFOS-preexposed group were increased significantly by Cd exposure. Significant decrease of the survival rates and body length of fish were observed at 10 dpf among the larvae that were previously exposed to PFOS. These results suggest that preexposure to PFOS could affect antioxidant defense mechanisms and potentially increase the toxicity of Cd on mRNA expression and enzyme activity level responses, as well as on survival or growth of individuals.
接触全氟辛烷磺酸（PFOS）已知会对水生生物的甲状腺产生相关的不良影响。由于抗氧化防御机制是甲状腺的关键功能之一，我们研究了 PFOS 预先暴露是否会破坏甲状腺功能并增强鱼类中镉（Cd）引起的氧化应激。斑马鱼胚胎在受精后 7 天内暴露于对照或 0.5mg/L PFOS 中，随后在受精后 10 天（dpf）再暴露于 0.038mg/L Cd(2+)或 PFOS 和 Cd 的混合物中 3 天。测量存活率、体长、与甲状腺功能和氧化应激相关的信使 RNA（mRNA）表达、甲状腺激素水平以及丙二醛和抗氧化酶活性。在 PFOS 预暴露组中观察到与甲状腺功能相关的 mRNAs（甲状腺激素受体-α[THRα]、甲状腺激素受体-β[THRβ]、造血表达同源盒[hhex]和配对盒基因 8[pax8]）显著下调和甲状腺素（T4）水平降低，表明 PFOS 预暴露会影响生命后期甲状腺的功能。在随后暴露于 Cd 或 PFOS 和 Cd 的混合物时，PFOS 预暴露组中某些与氧化应激相关的基因，如超氧化物歧化酶 1（sod1）和热休克蛋白 70（hsp70），显著上调。暴露于 Cd 会显著增加 PFOS 预暴露组的谷胱甘肽 S-转移酶活性和丙二醛水平。在先前暴露于 PFOS 的幼虫中，在 10 dpf 时观察到存活率和体长显著下降。这些结果表明，PFOS 预先暴露会影响抗氧化防御机制，并可能增加 Cd 对 mRNA 表达和酶活性水平反应以及个体存活或生长的毒性。
