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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Protective effect of royal jelly on fluoride-induced nephrotoxicity in rats via the some protein biomarkers signalling pathways: a new approach for kidney damage.
Introduction Protective effect of royal jelly (RJ) on fluoride-induced nephrotoxicity was investigated in this study. Methods 42 healthy male Wistar rats (n = 42, 8 weeks of age) were divided equally into 6 groups with 7 rats in each; (1) Group-1: Controls fed with standard diet; (2) Group-2: RJ [100 mg/kg] bw (body
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Hesperidin protects liver and kidney against sodium fluoride-induced toxicity through anti-apoptotic and anti-autophagic mechanisms.
Highlights Hesperidin prevented NaF-induced hepatotoxicity and nephrotoxicity. Hesperidin attenuated NaF-induced oxidative stress and inflammation. Hesperidin reduced NaF-induced apoptosis and autophagy. Aim High dose of fluoride intake is associated with toxic effects on liver and kidney tissues. One approach to tackle these toxicities is using natural antioxidants as supplements. This study evaluated
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Toxic effects of fluoride on kidney function and histological structure in young pigs
The effects of chronic fluoride exposure on kidney integrity and histological structure, along with effects on associated enzymes and metabolite changes, were investigated in young pigs. Twenty-four crossbred barrows (Duroc×Landrace×Yorkshire) about 50 days old were randomly divided into three groups of eight pigs each. Groups I, II, and III received
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Nephrotoxicity of chlorofluoroacetic acid in rats.
Dichloroacetic acid (DCA), chlorofluoroacetic acid (CFA), and difluoroacetic acid (DFA) are inhibitors of pyruvate dehydrogenase kinase. DCA is used for the clinical management of congenital lactic acidosis. Glutathione transferase zeta (GSTZ1-1) catalyzes the biotransformation of DCA and CFA, and DCA is a mechanism-based inactivator of GSTZ1-1. In rodents, DCA causes
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Effects of selenium intervention on chronic fluorosis-induced renal cell apoptosis in rats
This study aims to explore the effect of selenium in fluoride-induced renal cell apoptosis in rats and determine the optimal level of selenium in drinking water to prevent fluorosis. Experimental animals were divided into a control group, a sodium fluoride-treated group (NaF, 50 mg/L), three sodium selenite-treated groups (Na2SeO3, 0.375, 0.75,
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