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https://www.selleckchem.com/products/tak-875.html The environmental contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) causes hepatic toxicity associated with prominent lipid accumulation in humans. Here, the authors report that the lysosomal copper transporter SLC46A3 is induced by TCDD and underlies the hepatic lipid accumulation in mice, potentially via effects on mitochondrial function. SLC46A3 was localized to the lysosome where it modulated intracellular copper levels. Forced expression of hepatic SLC46A3 resulted in decreased mitochondrial membrane potential and abnormal mitochondria morphology consistent with lower copper levels. SLC46A3 expression increased hepatic lipid accumulation similar to the known effects of TCDD exposure in mice and humans. The TCDD-induced hepatic triglyceride accumulation was significantly decreased in Slc46a3-/- mice and was more pronounced when these mice were fed a high-fat diet, as compared to wild-type mice. These data are consistent with a model where lysosomal SLC46A3 induction by TCDD leads to cytosolic copper deficiency resulting in mitochondrial dysfunction leading to lower lipid catabolism, thus linking copper status to mitochondrial function, lipid metabolism and TCDD-induced liver toxicity.Magma from Plinian volcanic eruptions contains an extraordinarily large numbers of bubbles. Nucleation of those bubbles occurs because pressure decreases as magma rises to the surface. As a consequence, dissolved magmatic volatiles, such as water, become supersaturated and cause bubbles to nucleate. At the same time, diffusion of volatiles into existing bubbles reduces supersaturation, resulting in a dynamical feedback between rates of nucleation due to magma decompression and volatile diffusion. Because nucleation rate increases with supersaturation, bubble number density (BND) provides a proxy record of decompression rate, and hence the intensity of eruption dynamics. Using numerical modeling of bubble nucleation, we reconcile

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