Various authors have studied the effect of fluoride ion upon mammalian cells using many different biological end-points, of:which inhibition of the function of specific cellular enzymes, survival of cell reproductive capacity, production of abnormalities of cell division and alteration in the rate of cell proliferation are a representative sample. In this review the minimum fluoride ion concentration at which biological effects are detect- able are compared for each of these end-points. The usefulness of such in vitro studies for evaluation of potential whole-animal toxicity is discussed.
Selenium increases expression of HSP70 and antioxidant enzymes to lessen oxidative damage in Fincoal-type fluorosis
Fincoal type fluorosis has only been reported from China, but its pathogenesis is unclear. Many people believe that fluorosis is associated with oxidative stress. Oxidative stress can be reduced at higher selenium (Se) level. Heat shock protein (HSP70) is the most conserved and induced against different stressors. The aim of
The effects and underlying mechanism of excessive iodide on excessive fluoride-induced thyroid cytotoxicity
In many regions, excessive fluoride and excessive iodide coexist in groundwater, which may lead to biphasic hazards to human thyroid. To explore fluoride-induced thyroid cytotoxicity and the mechanism underlying the effects of excessive iodide on fluoride-induced cytotoxicity, a thyroid cell line (Nthy-ori 3-1) was exposed to excessive fluoride and/or excessive
Effects of fluoride on the intracellular free Ca2+ and Ca2+-ATPase of kidney.
In the present study, the effect of fluoride on intracellular free calcium ([Ca2+]i) and Ca2+-ATPase of renal cells were examined. Some paradoxical experimental results about the mechanism of fluoride toxicity were observed. In vivo, 48 Wistar rats were divided into 4 groups, and half of rats were treated with sodium
JNK and NADPH oxidase involved in fluoride-induced oxidative stress in BV-2 microglia cells.
Abstract Excessive fluoride may cause central nervous system (CNS) dysfunction, and oxidative stress is a recognized mode of action of fluoride toxicity. In CNS, activated microglial cells can release more reactive oxygen species (ROS), and NADPH oxidase (NOX) is the major enzyme for the production of extracellular superoxide in microglia. ROS
Dehydrogenase activity in the brain of fluoride and aluminium induced wistar rats
Dehydrogenases are cellular enzymes usually used as indicators of changes in cell activity and morphology; this includes metabolic processes such as structural differentiation, cell migration, cellular damage and even cell death; hence, assay of enzymes as Lactate dehydrogenase and Glucose 6 phosphate dehydrogenase could provide evidence for the role of
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