Abstract
An excess of sodium fluoride (135 mg F/kg body weight) was given in a single oral dose to male Wistar rats. Effects were investigated of fluoride-induced acute kidney intoxication on the time-dependent variations of urine volume. Also, of urinary fluoride ion (F-), alpha-glutathione-S-transferase (alpha-GST), N-acetyl-beta-D-glucosaminidase (NAG), and creatinine (CR) concentrations. Fluoride administration strongly affects these urinary biochemical indices. Of the several biomarkers studied, alpha-GST is particularly useful as marker of S3 proximal tubule damage. We found that alpha-GST shows the strongest and more durable changes as a result of the large dose of F- given to the experimental animals. Our results suggest that the toxic effect of F- on the kidney may be more pronounced in the proximal tubule than the glomeruli region, and that the disorder of the proximal tubule is more serious in the S3 segment than S1 or S2 segment. Alpha-GST proved to be a useful marker for the early detection and long-term observation of proximal renal tubular injury resulting from F- intoxication. The animal model should help to establish guidelines for the treatment of industrial workers suffering from acute renal failure resulting from accidental exposure to fluoride.
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Sodium fluoride induces apoptosis in the kidney of rats through caspase-mediated pathways and DNA damage
Long-term excessive sodium fluoride (NaF) intake can cause many bone diseases and nonskeletal fluorosis. The kidneys are the primary organs involved in the excretion and retention of NaF. The objective of the present study was to determine the effects of NaF treatment on renal cell apoptosis, DNA damage, and the
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Oxidative stress parameters in rats exposed to fluoride and caffeine
In our experiment, the 1-month effects of caffeine (Caff) and fluoride (F) administered separately and together on nitric oxide and total antioxidant status in serum, brain, liver and kidney of rats were investigated. Also, the influence of caffeine on fluoride excretion with urine was studied. Thirty adult male Wistar rats
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The mitochondrial pathway is involved in sodium fluoride (NaF)-induced renal apoptosis in mice.
The objective of the present study was to explore the molecular mechanism of apoptosis induced by sodium fluoride (NaF) in the mouse kidney by using the methods of flow cytometry, quantitative real-time polymerase chain reaction (qRT-PCR), western blotting, and experimental pathology. 240 four-week-old ICR mice were randomly divided into 4
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Fluoridation of drinking water and chronic kidney disease: absence of evidence is not evidence of absence.
Comment on Effects of fluoridation of community water supplies for people with chronic kidney disease. [Nephrol Dial Transplant. 2007, Oct;22(10):2763-7.] Sir, Ludlow et al. [1] only confirmed that our knowledge of the potential adverse effects of chronic low fluoride supplementation of drinking water on normal or diseased kidneys is insufficient. More than
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Histologic findings in the kidney, liver, pancreas, adrenal, and thyroid glands of the rat following sodium fluoride administration
1. Fluoride toxicosis was induced in young rats of the Long-Evans strain. Ten rats received a total of 406.47 mg. each of sodium fluoride injected intraperitoneally over a fifteen-day period, to induce acute poisoning. Seven rats survived, of which six were analyzed for this study. Ten others received a total
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