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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In Vivo Comparison of the Phenotypic Aspects and Molecular Mechanisms of Two Nephrotoxic Agents, Sodium Fluoride and Uranyl Nitrate.
Because of their nephrotoxicity and presence in the environment, uranium (U) and fluoride (F) represent risks to the global population. There is a general lack of knowledge regarding the mechanisms of U and F nephrotoxicity and the underlying molecular pathways. The present study aims to compare the threshold of the
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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.
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