Abstract
Although there are many studies on effect of fluoride on trace elements in experimental animals, few studies exist on serum trace elements levels in patients with endemic fluorosis. We aimed to determine the serum levels of trace elements including serum copper (Cu), zinc (Zn), and serum levels of minerals including calcium (Ca), phosphorus (P), magnesium (Mg), sodium (Na), potassium (K) in patients with endemic fluorosis. The study group consisted of 30 patients with endemic fluorosis (17 females, 13 males, mean age 33.53±9.85 years). An age, gender, and body mass index matched 30 healthy volunteers comprised control group (21 females, ten males with a mean age 33.93±7.39 years). Urine fluoride levels of chronic fluorosis patients were significantly higher than that of control subjects as expected (1.92±0.10 mg/l vs. 0.41±0.09 mg/l, respectively; P<0.001). Serum Cu levels (89.14±16.77 ?g/dL vs. 102.69±25.04 ?g/dL, respectively, P=0.017), serum Zn levels (77.98±20.58 ?g/dL vs. 94.57±35.87?g/dL, respectively, P=0.032), and serum Mg levels (1.92±0.18 mg/dL vs. 2.07±0.31 mg/dL, respectively, p=0.022) was significantly lower in chronic fluorosis patients than in controls. There were no statistically significant differences between the fluorosis group and control group with respect to serum levels of Na, K, Ca, and P. We concluded that chronic fluorosis is associated with reduced serum levels of Cu, Zn, and Mg.
-
-
Changes in basic metabolic elements associated with the degeneration and ossification of ligamenta flava
OBJECTIVE: To determine the association between levels of basic metabolic elements and degeneration and ossification of the ligamentum flavum (LF). SUBJECTS: Fourteen consecutive patients with degenerative lumbar stenosis, 11 with ossification of the thoracic ligamenta flava, and 11 control subjects. METHODS: The basic elements of calcium (Ca), phosphorus (P), magnesium (Mg), zinc
-
Influence of supplementary vitamins and minerals on lipid peroxidation and redox state in heart, kidney and liver of rats exposed to fluoride.
The effect of fluoride (F) and supplementary vitamins and minerals on lipid peroxidation (LPO) and redox state (RS) in heart , kidney and liver of 40 (4 groups of 10) male Wistar rats were studied. One group of rats was left untreated as control, group 1 was received 5 mg/l
-
Association Between Antioxidant Nutrients, Oxidative Stress-Related Gene Polymorphism and Skeletal Fluorosis in Guizhou, China.
Background: Oxidative stress plays an important role in the pathogenesis of endemic fluorosis. We analyzed associations between oxidative stress-related gene polymorphisms (PON1 rs662, CAT rs769217, rs2300182, and SOD2 rs11968525) and skeletal fluorosis, and examined potential gene–environment interactions with dietary vitamin C, vitamin E, zinc, and selenium intake. Methods: A cross-sectional study
-
Clinical aspects of fluorosis in horses
Horses grazing in areas where cattle and sheep had developed severe fluorosis were examined clinically. Of those examined, 12 horses of different ages and with various degrees of fluorosis were selected for necropsy. Selected tissues were examined grossly, histologically, and radiographically. Major fluorotic lesions occurred only when the horses ingested
-
Long-term exposure to the fluoride blocks the development of chondrocytes in the ducks: The molecular mechanism of fluoride regulating autophagy and apoptosis.
Highlights Long-term fluoride exposure blocks the development of chondrocytes. Excessive fluoride could induce chondrocytes apoptosis. Long-term excessive fluoride triggered autophagy. Fluoride-induced chondrocytes apoptosis is associated with CytC/Bcl-2/P53 pathways. Long-term exposure to excessive fluoride causes chronic damage in the body tissues and could lead to skeletal and dental fluorosis. Cartilage damage
Related Studies :
-
-
-
Skeletal Fluorosis in India & China
In India and China, scientists have repeatedly found that skeletal fluorosis occurs in populations drinking water with just 0.7 to 1.5 ppm fluoride. Although nutritional deficiencies and hot climates make populations in India and China more susceptible to fluoride toxicity than is generally the case in western countries, this fact does not remove the relevance of the Indian and Chinese experience to the situation in fluoridating countries. This is because (a) nutritional deficiencies also exist in the western world, particularly in low-income communities, and (b) some individuals, including those with kidney disease, can be just as -- if not more -- susceptible to fluoride toxicity.
-
Skeletal Fluorosis Causes Bones to be Brittle & Prone to Fracture
It has been known since as the early as the 1930s that patients with skeletal fluorosis have bone that is more brittle and prone to fracture. More recently, however, researchers have found that fluoride can reduce bone strength before the onset of skeletal fluorosis. Included below are some of the
-
Fluoride & Spinal Stenosis
Spinal stenosis is a narrowing of the spaces in the spine that results in pressure being placed on the spinal cord and/or nerve roots. Although stenosis can develop without symptoms, it may produce numbness, tingling, pain and difficulty in walking, as well as a heavy/tired feeling in the legs. It is estimated that 250,000 to 500,000 Americans currently have symptoms of spinal stenosis. Skeletal fluorosis is one cause of stenosis.
-
Gastrointestinal Problems Among Individuals with Skeletal Fluorosis
Humans suffering from skeletal fluorosis are known to suffer from an increased occurrence of gastrointestinal disorders. When fluoride intake is reduced, these gastrointestinal problems are among the first symptoms to disappear. The following are some of the studies that have examined this issue: "It is clear from the observations presented in this article
-
Variability in Radiographic Appearance of Skeletal Fluorosis
Osteosclerosis (dense bone) is the bone change typically associated with skeletal fluorosis, particularly in the axial skeleton (spine, pelvis, and ribs). Research shows, however, that skeletal fluorosis produces a spectrum of bone changes, including osteomalacia, osteoporosis, exostoses, changes resulting from secondary hyperparathyroidism, and combinations thereof. Although the reason for this radiographic variability is not yet fully understood, it is believed to relate to the dose of fluoride consumed, the individual's nutritional status, exposure to aluminum, genetic susceptibility, presence of kidney disease, and area of the skeleton examined.
Related FAN Content :
-