Abstract
Selective low (15 mg sodium fluoride (NaF)/L) and relatively high (150 mg NaF/L) doses of in vivo fluoride (F) treatment to Swiss albino mice through drinking water elicited organ-specific toxicological response. All the F-exposed groups showed severe alterations in both liver and kidney architectures, but there was no significant change in the rate of water consumption and body weight. Vacuolar degeneration, micronecrotic foci in the hepatocytes, and hepatocellular hypertrophy were evident in the mice exposed to low dose (15 mg NaF/L for 30 days) while sinusoidal dilation with enlarged central vein surrounded by deep-blue erythrocytes were preponderant when treated with the same dose for a period of 90 days. Blood filled spaces, disintegration of tubular epithelium, and atrophy of glomeruli were also recorded in the kidney of the same treatment group. Change in reduced glutathione level (GSH), glutathione-s-transferase (GST) activity, malondialdehyde (MDA) production in both liver and kidney, disturbances in liver function, induction of heat shock protein 70 (Hsp 70) expression in kidney and its down regulation in liver were positively correlated with histopathological lesion.
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Gaseous Anesthetics.
Introduction The history of anesthesia is a relatively recent one; if one begins with the analgesia dentist, Horace Wells, who discovered the used nitrous oxide during a dental extraction in the early 1800s. The first public showing of anesthesia occurred in October 1846, when ether was used to prevent pain during surgery
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Conceivable amelioration of NaF-induced toxicity in liver, kidney and brain of chicken by black tea extract: an in vitro study.
Sodium fluoride (NaF) toxicity on enzymatic and non-enzymatic oxidative stress markers of chicken liver, kidney and brain homogenate in in vitro condition where studied in present investigation. We studied alteration in the activity of superoxide dismutase (SOD), catalase (CAT), lipid peroxidation (LPO) and glutathione (GSH) content to study oxidative stress.
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Study on changes of clinical indicators and key proteins from fluoride exposure
Few studies have evaluated the biomarker changes of fluoride exposure. In order to explore early and sensitive indicators, animal experiment was designed. Ninety-six healthy SD rats (48 males and 48 females) weighing approximately 60 g were randomly divided into six groups of 16 animals each by gender average. Control animals
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[An investigation on the effect of Rosa roxburghii tratt juice on chronic fluorosis and its mechanism].
Improved the general condition of chronic fluorosis but had no effect on dental fluorosis enhanced the excretion of fluorine and lowered the fluorine content of serum and bone which has been raised during fluorine intoxication; increased serum vitamin C and protected collagen as manifested by declin[e] of urinary hydroxyproline; inhibited
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Studies on effects of fluoride in 36 villages of Mehsana District, North Gujurat"
A survey was carried out in 36 fluoride endemic villages of Mehsana District of North Gujarat. Urine and blood samples of fluoride-afflicted human population and their drinking water were analysed for fluoride content and compared with samples from different parts of Ahmedabad city (control). The fluoride content in water samples
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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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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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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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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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