Abstract
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 the same basal diet additionally supplemented, respectively, with 0, 100, and 250 mg F–/kg (from NaF). Results obtained after 50 days indicated that supplemental fluoride-treatment caused severe renal histological changes as well as increased renal cell apoptosis. In kidney tissue, lactate dehydrogenenase (LDH) activity was significantly increased in group III, whereas alkaline phosphatase (AKP) activity was significantly decreased in group II as well as in group III. In the serum, significantly increased urea nitrogen (UN) was present in groups II and III, and the serum of group III had elevated creatinine (Cre) and decreased Na+. These findings show that chronic excessive fluoride exposure is deleterious to kidney structure and function of pigs.
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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 and zinc on renal oxidative stress and apoptosis induced by fluoride in rats.
OBJECTIVE: To study the effects of selenium and zinc on oxidative stress, apoptosis, and cell cycle changes in rat renal cells induced by fluoride. METHODS: Wistar rats were given distilled water containing sodium fluoride (50 mg/L NaF) and were gavaged with different doses of selenium-zinc preparation for six months. Four groups
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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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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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Effect of sodium fluoride on the expression of Bcl-2 family and osteopontin in rat renal tubular cells
Our earlier studies showed that the apoptosis of renal tubules can be induced by sodium fluoride (NaF). The present study was designed to estimated the effects of B-cell lymphoma/leukemia 2 (Bcl-2), Bcl-2-associated protein X (Bax), and osteopontin (OPN) on the apoptosis of renal tubular cells induced by NaF at different
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Fluoride as a Cause of Kidney Disease in Animals
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the exception of the pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease - thus initiating a "vicious cycle" where the damaged kidneys increase the accumulation of fluoride, causing in
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Kidney: A potential target for fluoride toxicity
The kidneys are the organ responsible for clearing fluoride from the body. In the process of doing so, the kidneys are exposed to concentrations of fluoride that exceed, by a factor of 50, the concentration of fluoride in human blood. As such, the kidney have long been considered a potential
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Fluoridation of drinking water and chronic kidney disease: Absence of evidence is not evidence of absence
A fairly substantial body of research indicates that patients with chronic renal insufficiency are at an increased risk of chronic fluoride toxicity. Patients with reduced glomerular filtration rates have a decreased ability to excrete fluoride in the urine. These patients may develop skeletal fluorosis even at 1 ppm fluoride in the drinking water.
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Fluoride as a Cause of Kidney Disease in Humans
Because the kidney is exposed to higher concentrations of fluoride than all other soft tissues (with the exception of the pineal gland), there is concern that excess fluoride exposure may contribute to kidney disease - thus initiating a "vicious cycle" where the damaged kidneys increase the accumulation of fluoride, causing
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Fluoride & Kidney Stones
It has long been suspected that fluoride may contribute to the formation of kidney stones. This suspicion has recently gained support from a study of an American man with skeletal fluorosis. According to the authors: "A new, important, medical problem (that seemed temporally related to cessation of fluoride exposure and subsequent negative calcium
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