Abstract
OBJECTIVE: To study the relationship between death receptor pathway, mitochondrion pathway and fluoride-induced apoptosis of renal cell.
METHODS: Male Sprague-Dawley rats were divided randomly into four groups (control, low-fluoride, medium-fluoride,and high-fluoride) and administered 0, 50, 100, and 200 mg/L of sodium fluoride, respectively, via drinking water for 120 days. The incidence of dental fluorosis were observed, the body weights and urine fluoride levels were measured. Apoptosis was detected by the Flow Cytometry (FCM). The expressions of protein of Caspase-3, Caspase-8, Caspase-9, Cyt C were detected by immunohistoehemistry.
RESULTS: The apoptosis rate in the fluoride exposed low does group, middle dose group and high dose group increased significantly as compared with control group. The average optical density value of Caspase-3, Caspase-8, Caspase-9 and Cyt C were higher in the fluoride exposed middle dose group and high dose group than those in the control group (P < 0.05).
CONCLUSION: Death receptor pathway and mitochondrion pathway may participate in the process of fluoride-induced apoptosis of renal cell.
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Fluorosis caused cellular apoptosis and oxidative stress of rat kidneys
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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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Effects of selenium intervention on chronic fluorosis-induced renal cell apoptosis in rats
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Toxic effects of fluoride on kidney function and histological structure in young pigs
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