Oncü Meral, Kocak Ahmet, Karaoz Erdal, Darici Hakan, Savik Emin, Gultekin Fatih
Department of Histology and Embryology, Faculty of Medicine, Suleyman Demirel University, Morfoloji Binasi, Isparta 32040, Turkey.
Biol Trace Elem Res. 2007 Sep;118(3):260-8. doi: 10.1007/s12011-007-0036-6.
This experiment was designed to investigate the histological and lipid peroxidation effects of chronic fluorosis on testes tissues of first- and second-generation rats. Sixteen virgin female Wistar rats were mated with eight males (2:1) for approximately 12 h to obtain first-generation rats. Pregnant rats were divided into two groups: controls and fluoride-given group, each of which containing five rats. Pregnant rats in the fluoride-given group were exposed to a total dose of 30 mg/l sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/l of NaF throughout the gestation and lactation periods. After the lactation period, the young animals (first generation, F1) were exposed to the same dose of NaF in drinking water for 4 months. At the end of the 4 months of experimental period, nine randomly chosen male rats (F1) were killed and testes tissues were taken for histopathological and biochemical analysis. The remaining eight female rats were mated with four males (2:1) for approximately 12 h to obtain second-generation rats. Six female were identified as pregnant and treated with similarly throughout the gestation and the lactation periods. After the lactation period, the young male animals (second generation, F2) were also treated in the same way for 4 months. At the end of the 4 months of experimental period, nine randomly chosen male rats (F2) were killed and testes tissues were collected for histopathological and biochemical analysis. The rats in the control group were applied the same procedure without NaF administration. In biochemical analysis of the fluoride given F1 and F2 rats, it has been found that plasma fluoride levels and testes thiobarbituric acid reactive substance levels were significantly increased when compared with the control group. In F1 and F2 rats, similar histopathological changes were observed. In both groups, spermatogenesis was severely reduced. Spermatogonia and primary spermatocytes were normal, however, there was a widespread degeneration in other spermatogenic cell lines of the seminiferous epithelium. The histological structures of the Sertoli and interstitial Leydig cells were normally observed. It is concluded that chronic fluorosis exposure leads to a remarkable destruction in testes tissues of F1 and F2 rats via lipid peroxidation.
本实验旨在研究慢性氟中毒对第一代和第二代大鼠睾丸组织的组织学及脂质过氧化作用。16只未孕雌性Wistar大鼠与8只雄性大鼠(2:1)交配约12小时以获得第一代大鼠。将怀孕大鼠分为两组:对照组和给予氟化物组,每组各有5只大鼠。给予氟化物组的怀孕大鼠在整个妊娠期和哺乳期饮用含0.07 mg/l氟化钠(NaF)的商业饮用水,其中总氟含量为30 mg/l。哺乳期结束后,幼崽(第一代,F1)饮用相同剂量的含氟饮用水4个月。在4个月实验期结束时,随机选取9只雄性大鼠(F1)处死,取出睾丸组织进行组织病理学和生化分析。其余8只雌性大鼠与4只雄性大鼠(2:1)交配约12小时以获得第二代大鼠。6只雌性大鼠确认怀孕,并在整个妊娠期和哺乳期进行同样的处理。哺乳期结束后,幼崽雄性动物(第二代,F2)也以同样方式处理4个月。在4个月实验期结束时,随机选取9只雄性大鼠(F2)处死,收集睾丸组织进行组织病理学和生化分析。对照组大鼠采用相同程序,但不给予NaF。在对给予氟化物的F1和F2大鼠进行生化分析时发现,与对照组相比,血浆氟水平和睾丸硫代巴比妥酸反应物质水平显著升高。在F1和F2大鼠中观察到类似的组织病理学变化。两组中,精子发生均严重减少。精原细胞和初级精母细胞正常,然而,生精上皮的其他生精细胞系存在广泛退化。支持细胞和间质莱迪希细胞的组织结构正常。结论是,慢性氟暴露通过脂质过氧化导致F1和F2大鼠睾丸组织显著破坏。