Karaoz Erdal, Oncu Meral, Gulle Kanat, Kanter Mehmet, Gultekin Fatih, Karaoz Sureyya, Mumcu Ethem
Kocaeli University, Health High School, Kocaeli, Turkey.
Biol Trace Elem Res. 2004 Winter;102(1-3):199-208. doi: 10.1385/BTER:102:1-3:199.
This experiment was designed to investigate the lipid peroxidation and histological effects of chronic fluorosis on first- and second-generation rat kidney tissues. Sixteen virgin female Wistar rats were mated with eight males (2: 1) for approx 12 h to obtain first-generation rats. Mating was confirmed by the presence of sperm in vaginal smears. Sperm in vaginal smears was observed in 10 of 16 rats (d 0). These rats were identified as pregnant and included in this experiment. Pregnant rats were divided into two experimental groups (control and fluoride-supplemented), each containing five rats. The pregnant rats in the fluoride-supplemented group were exposed to 30 mg/L sodium fluoride (NaF) in commercial drinking water containing 0.07 mg/L NaF throughout the gestation and the lactation periods. After the lactation period, young animals (first generation [F1]) were exposed to the same amount of NaF in drinking water for 4 mo. At the end of the 4-mo experimental period, nine randomly chosen male rats (F1) were sacrificed, and the kidneys were removed for the histological and lipid peroxidation examinations. The remaining eight female rats were mated with four males (2: 1) for approx 12 h to obtain second-generation rats. Six female were identified as pregnant, and treated similarly throughout the gestation and the lactation periods. After the lactation period, the young male rats (second-generation male rats [F2]) were also treated similarly for 4 mo. At the end of the 4-mo experimental period, nine randomly chosen male rats (F2) were sacrificed, and the kidneys were removed for the histological and lipid peroxidation examinations. The rats in the control groups underwent the same procedure without NaF supplementation. It was found that the plasma fluoride and kidney TBARS levels of fluoride-supplemented F1 and F2 rats were higher than controls. Hydropic epithelial cell degenerations and moderate tubular dilatation were observed in some proximal and distal tubules. There were markedly focal mononuclear cell infiltrations and hemorrhage at some areas of the interstitium, especially at the corticomedullar junction. Mononuclear cell infiltrations were also evident in some peritubular and perivascular areas. Most of the vascular structures were congestive. Many Bowman capsules were narrowed. The severe degenerative changes in most of the shrunken glomerules and vascular congestion were also observed.
本实验旨在研究慢性氟中毒对第一代和第二代大鼠肾脏组织的脂质过氧化及组织学影响。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。通过阴道涂片中有精子来确认交配。16只大鼠中有10只(第0天)阴道涂片观察到精子。这些大鼠被确定为怀孕并纳入本实验。怀孕大鼠分为两个实验组(对照组和补充氟组),每组各有5只大鼠。补充氟组的怀孕大鼠在整个妊娠期和哺乳期饮用含0.07mg/L氟化钠(NaF)的市售饮用水,并添加30mg/L氟化钠。哺乳期结束后,幼崽(第一代[F1])饮用相同量含NaF的饮用水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,取出肾脏进行组织学和脂质过氧化检查。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只雌性大鼠被确定为怀孕,并在整个妊娠期和哺乳期进行同样处理。哺乳期结束后,幼崽雄性大鼠(第二代雄性大鼠[F2])也同样处理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,取出肾脏进行组织学和脂质过氧化检查。对照组大鼠进行相同操作,但不补充NaF。结果发现,补充氟的F1和F2大鼠血浆氟和肾脏丙二醛水平高于对照组。在一些近端和远端小管观察到上皮细胞水肿变性和中度肾小管扩张。间质的一些区域,特别是皮质髓质交界处,有明显的局灶性单核细胞浸润和出血。在一些肾小管周围和血管周围区域也可见单核细胞浸润。大多数血管结构充血。许多肾小囊变窄。还观察到大多数萎缩肾小球有严重的退行性改变和血管充血。