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. It is concluded that chronic fluorosis causes a marked destruction in kidney tissues of F1 and F2 rats by causing lipid peroxidation.