羟基酪醇拮抗PFOS雄性小鼠生殖损害作用

Antagonism of hydroxytyrosol on male reproductive toxicity of PFOS

目的探讨羟基酪醇对全氟新烷磺酸(PFOS)所致雄性小鼠生殖损害的拮抗作用。方法 50只雄性昆明系小鼠随机分成对照组、PFOS组及PFOS+羟基酪醇低、中、高(12.5、25.0、50.0 mg/L)组,通过饮水加PFOS、羟基酪醇的方法染毒35 d,观察小鼠精子计数、活动率及畸形率、睾丸生化标志酶、血清性激素水平以及氧化应激指标的改变。结果低、中、高剂量羟基酪醇组小鼠精子数量分别为21.01×107、22.76×107、23.76×107个/g附睾,精子活动率分别为55.24%、71.03%、83.19%,与PFOS组比较,精子数量增多,精子活动率升高;与PFOS组比较,中、高剂量羟基酪醇组小鼠乳酸脱氢酶(LDH)、碱性磷酸酶(ALP)、促黄体生成素(LH)和血清睾酮(T)水平均有不同程度升高(P<0.05),各剂量羟基酪醇组超氧化物歧化酶(SOD)和过氧化氢酶(CAT)活力升高、丙二醛(MDA)含量降低,差异均有统计学意义(P<0.05)。结论羟基酪醇可以拮抗PFOS所致的小鼠雄性生殖功能损伤,其主要机制可能与氧化应激和性激素调节有关。

Objective To study the antagonism of hydroxytyrososl（HT） on male reproductive toxicity induced by peffluorooctane sulfonate （ PFOS ）. Methods Totally 50 male mice were randomly divided into five groups ： control group, PFOS group （ 25.0 mg/L）, PFOS （ 25.0 mg/L ） plus low-dose HT （ 12. 5mg/L ）, PFOS （ 25.0 mg/L ） plus midium-dose HT（ 25.0 rag/L） , and PFOS （ 25.0 mg/L） plus high-dose HT （ 50. 0 mg/L ） groups. After the animals were fed with deionized water supplemented with PFOS or/and HT for 35 days, the count of sperm and the rates of spermmobility and aberration were analyzed;the levels of lactate dehydrogenase （LDH）, alkaline phosphatase （ALP）, ser- um testosterone （ T ）, and luteinizing hormone （ LH ） were examined; meanwhile catalase （ CAT ）, superoxide dismutase （SOD） enzyme and the change of malondialdehyde （MDA） content were detected. Results The number of sperm in rats of low ,medium,and high dose of HT groups increased significantly（21.01,22. 76 ,and 23.76 × 10^7/g epididymis） compared with that of PFOS exposure groups. In addition,the sperm motility increased（55.24% ,71.03% ,and 83.19% ） and the sperm deformity rate decreased. The levels of LDH, ALP, serum T, and LH of medium and high HT groups increased （ P 〈 0. 05 for all） compared to those of PFOS group. The low, medium and high doses of HT recovered the activities of SOD and CAT enzyme,lowered MDA content obviously compared with PFOS groups, with significant differences （ P 〈 0. 05 for all）. Conclusion HT can inhibit the damage of reprouductive function induced by PFOS. Reducing oxidative damage and regulating secretion of testosterone and LH are important mechanisms of the effect.