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The fluoride permeation pathway and anion recognition in Fluc family fluoride channels.

Introduction Microbes are protected from the cytoplasmic accumulation of environmental fluoride ion by export of the toxic anion via fluoride channels known as Flucs [1-3]. These small, homodimeric ion channels are remarkable proteins in two regards: first, their unusual “dual topology” architecture, in which the two subunits of the homodimer are arranged antiparallel with respect to each other [4,5], yielding a double-barreled pair of pores related by two-fold symmetry [6-9]. Second, the F

Gut microbiota perturbations and neurodevelopmental impacts in offspring rats concurrently exposure to inorganic arsenic and fluoride.

3.3. Effects of iAs and F-, alone or in combination, on pathological changesin the hippocampal CA1 region H&E staining of neuron in the hippocampal CA1 region was observed at different optical microscope magnifications (Bar = 100 um 50 um in Fig. 2B & C respectively). In the control group, hippocampal CA1 neurons were tightly organized and had multiple cell layers, with healthy cell morphology and clearly stained nuclei and nucleoli. Compared with the control group, hippocampal CA1 neur

Chemical pathology of homocysteine. IV. Excitotoxicity, oxidative stress, endothelial dysfunction, and inflammation.

Fluoride is a toxic anion that stimulates oxygen consumption [64] and increases superoxide production in resting polymorphonuclear leukocytes [65]. Intracellular calcium ions are required for superoxide production by neutrophils during phagocytosis [66]. The effect of fluoride on superoxide production in neutrophils is reversible, causing superoxide production in the presence of fluoride, decreasing superoxide production when fluoride is removed, and restoring superoxide production when fluoride