Abstract

Blood samples from 24 adult males, age 25 to 40, with endemic skeletal fluorosis, living in the Vaillapally village of the Nalgonda district, Andhra Pradesh, India, were examined and compared with samples from 15 matched controls for their antioxidant enzyme activity and lipid peroxidation. Elevated malondialdehyde (MDA) levels indicated an increase in lipid peroxidation products, and decreased activity levels of catalase (CAT) and glutathione-S-transferase (GST) reflected significant alterations in their antioxidant status. These results, in agreement with recent findings by others, demonstrate that chronic fluoride intoxication in adult males elicits increased lipid peroxidation associated with a significant decrease in the activities of CAT and GST.

• Related Studies :

  • Fluoride in Drinking Water and Skeletal Fluorosis: a Review of the Global Impact.

    When safe and adequate exposure of an essential trace element is exceeded it becomes potentially toxic. Fluoride is one classic example of such a double edged sword which both plays a fundamental role in the normal growth and development of the body for example the consumption of levels between 0.5–1.0 ppm

  • Fluoride-induced oxidative stress in three-dimensional culture of OS732 cells and rats.

    Exposure to excessive fluoride poses a threat to human health, including increased susceptibility to developing the skeletal fluorosis. Despite its recognized importance as an endemic disease, little is known about how fluoride directly impacts on osteoblasts. We previously reported that fluoride-stimulating monolayer-cultured osteoblast proliferation or inhibiting cell viability depended on

  • Effect of fluoride on oxidative stress and biochemical markers of bone turnover in postmenopausal women

    The present study was conducted on 42 postmenopausal women subjects in Vailapally village, Nalgonda district, Andhra Pradesh, India, an endemic fluorotic area (water fluoride >4 ppm) and 34 postmenopausal women of nonfluorotic villages (water fluoride <0.4 ppm) of the Nalgonda area. The age group of the recruited subjects was 48–58

  • 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

  • [Effect of endemic fluoride poisoning caused by coal burning on the oxidative stress in rat testis].

    OBJECTIVE:  To explore the effect of endemic fluoride poisoning caused by coal burning on the oxidative stress in rat testis. METHODS:  Totally 40 male SD rats were equally randomized into four groups control group, low fluorosis group, middle fluorosis group, and high fluorosis group. Rats in all three fluorosis groups were

• Related FAN Content :

  • Skeletal Fluorosis: The Misdiagnosis Problem

    It is a virtual certainty that there are individuals in the general population unknowingly suffering from some form of skeletal fluorosis as a result of a doctor's failure to consider fluoride as a cause of their symptoms. Proof that this is the case can be found in the following case reports of skeletal fluorosis written by doctors in the U.S. and other western countries. As can be seen, a consistent feature of these reports is that fluorosis patients--even those with crippling skeletal fluorosis--are misdiagnosed for years by multiple teams of doctors who routinely fail to consider fluoride as a possible cause of their disease.

  • Fluoride & Osteoarthritis

    While the osteoarthritic effects that occurred from fluoride exposure were once considered to be limited to those with skeletal fluorosis, recent research shows that fluoride can cause osteoarthritis in the absence of traditionally defined fluorosis. Conventional methods used for detecting skeletal fluorosis, therefore, will fail to detect the full range of people suffering from fluoride-induced osteoarthritis.

  • "Pre-Skeletal" Fluorosis

    As demonstrated by the studies below, skeletal fluorosis may produce adverse symptoms, including arthritic pains, clinical osteoarthritis, gastrointestinal disturbances, and bone fragility, before the classic bone change of fluorosis (i.e., osteosclerosis in the spine and pelvis) is detectable by x-ray. Relying on x-rays, therefore, to diagnosis skeletal fluorosis will invariably fail to protect those individuals who are suffering from the pre-skeletal phase of the disease. Moreover, some individuals with clinical skeletal fluorosis will not develop an increase in bone density, let alone osteosclerosis, of the spine. Thus, relying on unusual increases in spinal bone density will under-detect the rate of skeletal fluoride poisoning in a population.

  • Fluoridation, Dialysis & Osteomalacia

    In the 1960s and 1970s, doctors discovered that patients receiving kidney dialysis were accumulating very high levels of fluoride in their bones and blood, and that this exposure was associated with severe forms of osteomalacia, a bone-softening disease that leads to weak bones and often excruciating bone pain. Based on

  • Kidney Patients Are at Increased Risk of Fluoride Poisoning

    It is well established that individuals with kidney disease are susceptible to suffering bone damage and other ill effects from low levels of fluoride exposure. Kidney patients are at elevated risk because when kidneys are damaged they are unable to efficiently excrete fluoride from the body. As a result, kidney patients