Wei Ruifen, Luo Guangying, Sun Zilong, Wang Shaolin, Wang Jundong
Shanxi Key Laboratory of Environmental Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi 030801, China; School of Optometry and Ophthalmology and Eye Hospital, Wenzhou Medical University, 270 Xueyuan Road, Wenzhou, Zhejiang 325027, China.
Shanxi Key Laboratory of Environmental Veterinary Medicine, Shanxi Agricultural University, Taigu, Shanxi 030801, China.
Chemosphere. 2016 Jun;153:419-25. doi: 10.1016/j.chemosphere.2016.03.045. Epub 2016 Mar 28.
Previous studies have indicated that fluoride (F) can affect testicular toxicity in humans and rodents. However, the mechanism underlying F-induced testicular toxicity is not well understood. This study was conducted to evaluate the sperm quality, testicular histomorphology and inflammatory response in mice followed F exposure. Healthy male mice were randomly divided into four groups with sodium fluoride (NaF) at 0, 25, 50, 100 mg/L in the drinking water for 180 days. At the end of the exposure, significantly increased percentage of spermatozoa abnormality was found in mice exposed to 50 and 100 mg/L NaF. Disorganized spermatogenic cells, vacuoles in seminiferous tubules and loss and shedding of sperm cells were also observed in the NaF treated group. In addition, chronic F exposure increased testicular interleukin-17(IL-17), interleukin-17 receptor C (IL-17RC), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in transcriptional levels, as well as IL-17 and TNF-α levels in translational levels. Interestingly, we observed that F treated group elevated testicular inducible nitric oxide synthase (iNOS) mRNA level and nitric oxide (NO) concentration. Taken together, these results indicated that testicular inflammatory response could contribute to chronic F exposure induced testicular toxicity in mice.
以往研究表明,氟化物(F)可影响人类和啮齿动物的睾丸毒性。然而,F诱导睾丸毒性的潜在机制尚不清楚。本研究旨在评估氟暴露后小鼠的精子质量、睾丸组织形态学和炎症反应。将健康雄性小鼠随机分为四组,饮用含0、25、50、100mg/L氟化钠(NaF)的水180天。暴露结束时,发现暴露于50和100mg/L NaF的小鼠精子异常百分比显著增加。在NaF处理组中还观察到生精细胞紊乱、生精小管空泡形成以及精子细胞丢失和脱落。此外,慢性氟暴露使睾丸白细胞介素-17(IL-17)、白细胞介素-17受体C(IL-17RC)、肿瘤坏死因子-α(TNF-α)和白细胞介素-6(IL-6)的转录水平升高,以及IL-17和TNF-α的翻译水平升高。有趣的是,我们观察到F处理组睾丸诱导型一氧化氮合酶(iNOS)mRNA水平和一氧化氮(NO)浓度升高。综上所述,这些结果表明睾丸炎症反应可能导致慢性氟暴露诱导的小鼠睾丸毒性。