Many factors could potentially affect the process of arsenic-induced liver fibrosis. The present study was undertaken to examine the effect of high fat diet on arsenic-induced liver fibrosis and preneoplastic changes. Mice were given sodium arsenite (As3+, 200 ppm) or sodium arsenate (As5+, 200 ppm) in the drinking water for 10 months, and provided a normal diet or a diet containing 20% added fat. Serum aspartate aminotransferase (AST), indicative of liver injury, was elevated in both arsenite and arsenate groups, and a high fat diet further increased these levels. Histopathology (H&E and Masson stain) showed that liver inflammation, steatosis (fatty liver), hepatocyte degeneration, and fibrosis occurred with arsenic alone, but their severity was markedly increased with the high fat diet. Total liver RNA was isolated for real-time RT-PCR analysis. Arsenic exposure increased the expression of inflammation genes, such as TNF-alpha, IL-6, iNOS, chemokines, and macrophage inflammatory protein-2. The expression of the stress-related gene heme oxygenase-1 was increased, while metallothionein-1 and GSH S-transferase-pi were decreased when arsenic was combined with the high fat diet. Expression of genes related to liver fibrosis, such as procollagen-1 and -3, SM-actin and TGF-beta, were synergistically increased in the arsenic plus high fat diet group. The expression of genes encoding matrix metalloproteinases (MMP2, MMP9) and tissue inhibitors of metalloproteinases (TIMP1, TIMP2) was also enhanced, suggestive of early oncogenic events. In general, arsenite produced more pronounced effects than arsenate. In summary, chronic inorganic arsenic exposure in mice produces liver injury, and a high fat diet markedly increases arsenic-induced hepatofibrogenesis.

a b s t r a c tFlotation has been used in industry for more than a half century as the primary technique for upgrading phosphate. While the flotation of phosphate was inefficient when oleic acid was used alone as a collector, therefore a mixed collector of oleic acid (HOl), linoleic acid (LA) and linolenic acid (LNA) was employed to improve the recovery of phosphate flotation. The batch flotation results showed that the optimal composition of the mixed collector was 54 wt.% HOl, 36 wt.% LA and 10 wt.% LNA. Additionally, the effect of pH on the mixed collector application was studied while considering the surface tension, contact angle and micro-flotation. The results showed that the mixed collector should be used at a pH of 9.5. Above a pH of 9.5, the adsorption of fatty acids dimers on the apatite surface hindered phosphate flotation. The influence of the mixed collector assembly on apatite flotation was also investigated. It was demonstrated that due to its low critical micelle concentration, a sufficiently hydrophobic apatite surface could be generated at a collector concentration of 60 mg/L. In addition, zeta potential experiments suggested that collector adsorption was governed by chemisorption. FTIR and XPS spectra studies further indicated that the chemical reaction involved the carboxyl groups of fatty acids and Ca species at the apatite surface for each fatty acid in the mixed collector.

No abstract

No abstract

No abstract

No abstract

No abstract

First time to report mechanisms of polymethoxyflavone demethylation during citrus peel drying, as well as effects of different drying processes.