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Background: Lipotoxicity causes endoplasmic reticulum (ER) stress, leading to cell apoptosis. Sirtuin 1 (Sirt1) regulates gene transcription and cellular metabolism. In this study, we investigated the role of Sirt1 in palmitate-induced ER stress. Methods: Both H9c2 myoblasts and heart-specific Sirt1 knockout mice fed a palmitate-enriched high-fat diet were used. Results: The high-fat diet induced C/EBP homologous protein (CHOP) and activating transcription factor 4 (ATF4) expression in both Sirt1 knockout mice and controls. The Sirt1 knockout mice showed higher CHOP and ATF4 expression compared to those in the control. Palmitic acid (PA) induced ATF4 and CHOP expression in H9c2 cells. PA-treated H9c2 cells showed decreased cytosolic NAD+/NADH alongside reduced Sirt1′s activity. The H9c2 cells showed increased ATF4 and CHOP expression when transfected with plasmid encoding dominant negative mutant Sirt1. Sirt1 activator SRT1720 did not affect CHOP and ATF4 expression. Although SRT1720 enhanced the nuclear translocation of ATF4, the extent of the binding of ATF4 to the CHOP promoter did not increase in PA treated-H9c2 cells. Conclusion: PA-induced ER stress is mediated through the upregulation of ATF4 and CHOP. Cytosolic NAD+ concentration is diminished by PA-induced ER stress, leading to decreased Sirt1 activity. The Sirt1 activator SRT1720 promotes the nuclear translocation of ATF4 in PA-treated H9c2 cells.

Background: Lipotoxicity causes endoplasmic reticulum (ER) stress, leading to cell apoptosis. Sirtuin 1 (Sirt1) regulates gene transcription and cellular metabolism. In this study, we investigated the role of Sirt1 in palmitate-induced ER stress. Methods: H9c2 myoblasts and heart-specific Sirt1 knockout mice fed a palmitate-enriched high-fat diet were used. Results: The high-fat diet induced C/EBP homologous protein (CHOP) and activating transcription factor 4 (ATF4) expression in both Sirt1 knockout mice and controls. Sirt1 knockout mice showed higher CHOP and ATF4 expression compared to those in control. Palmitic acid (PA) induced ATF4 and CHOP expression in H9c2 cells. PA-treated H9c2 cells showed decreased cytosolic NAD+/NADH alongside reduced Sirt1’s activity. H9c2 cells showed increased ATF4 and CHOP expression when transfected with plasmid encoding dominant negative mutant Sirt1. Sirt1 activator SRT1720 did not affect CHOP and ATF4 expression. Although SRT1720 enhanced nuclear translocation of ATF4, the extent of the binding of ATF4 to the CHOP promoter did not increase further in PA treated-H9c2 cells.Conclusion: PA-induced ER stress is mediated through upregulation of ATF4 and CHOP. Cytosolic NAD+ concentration is diminished by PA-induced ER stress, leading to decreased Sirt1 activity. The Sirt1 activator SRT1720 promotes nuclear translocation of ATF4 in PA-treated H9c2 cells.

Sediments sampled from the Pearl River tributary inlet, with seriously black and odor problem, was treated with calcium nitrate injection in the river simulator. During the course, release and transformation of nitrogen from sediments was investigated. The results showed that calcium nitrate injection is one kind of feasible approaches for sediments odor control. Removal rate of sulfide in sediments reached up to 99% in a month, the color of sediments turned to light brown from black, and the odor disappeared. However, release of NH4+-N and NO3--N was accelerated with calcium nitrate injection, the maximum release concentration of NH4-N and NO3-N was close to 48 mg/L and 417.4 mg/L with injecting dosing of 8%(W/W, dry-weight). Furthermore, continued aeration to overlying water seemed not to be a good way for NO3-N removal. Contrastively, under low DO condition, both concentration of NH4-N and NO3-N took increasing-decrease trends. In this work, TN concentration decreased from 97.7 mg/L to 27.4 mg/L. That is, by maintaining low DO concentration in sediment-water interface, the extra release of nitrogen caused by calcium nitrate injection could be well controlled.

This is the first time to described the dissimilatory Fe(III) reducing characteristics of Shewanella cinica D14T. The effects of O2, light, temperature and pH on dissimilatory Fe(III) reduction were examined. The results suggested that the rate of Fe(III) reduction decreased with increasing Fe(III) concentration. Fe(III) reduction was partially inhibited by the presence of either O2 or light. The optimum temperature for Fe(III) reduction is 37 degrees C. At pH 6.0-10.0, strain D14T can reduce Fe(III). The soluble Fe(III) is more easy to be reduced than the insoluble one. Results of protein denaturants SDS and OGP suggest that the Fe(III) reduction activity of S. cinica is mostly localized to the soluble outer membrane fraction. The azo dye decolorization and Fe(III) reduction in strain D14T were enhanced in the presence of Fe(III) and dye.