Characterization and performance of carbonaceous materials obtained from exhausted sludges for the anaerobic biodecolorization of the azo dye Acid Orange II.

This work presents the preliminary study of new carbonaceous materials (CMs) obtained from exhausted sludge, their use in the heterogeneous anaerobic process of biodecolorization of azo dyes and the comparison of their performance with one commercial active carbon. The preparation of carbonaceous materials was conducted through chemical activation and carbonization. Chemical activation was carried out through impregnation of sludge-exhausted materials with ZnCl2 and the activation by means of carbonization at different temperatures (400, 600 and 800°C). Their physicochemical and surface characteristics were also investigated. Sludge based carbonaceous (SBC) materials SBC400, SBC600 and SBC800 present values of 13.0, 111.3 and 202.0m(2)/g of surface area. Biodecolorization levels of 76% were achieved for SBC600 and 86% for SBC800 at space time (τ) of 1.0min, similar to that obtained with commercial activated carbons in the continuous anaerobic up-flow packed bed reactor (UPBR). The experimental data fit well to the first order kinetic model and equilibrium data are well represented by the Langmuir isotherm model. Carbonaceous materials show high level of biodecolorization even at very short space times. Results indicate that carbonaceous materials prepared from sludge-exhausted materials have outstanding textural properties and significant degradation capacity for treating textile effluents.

Dose response of endotoxin on hepatocyte and muscle mitochondrial respiration in vitro.

INTRODUCTION Results on mitochondrial dysfunction in sepsis are controversial. We aimed to assess effects of LPS at wide dose and time ranges on hepatocytes and isolated skeletal muscle mitochondria. METHODS Human hepatocellular carcinoma cells (HepG2) were exposed to placebo or LPS (0.1, 1, and 10 μg/mL) for 4, 8, 16, and 24 hours and primary human hepatocytes to 1 μg/mL LPS or placebo (4, 8, and 16 hours). Mitochondria from porcine skeletal muscle samples were exposed to increasing doses of LPS (0.1-100 μg/mg) for 2 and 4 hours. Respiration rates of intact and permeabilized cells and isolated mitochondria were measured by high-resolution respirometry. RESULTS In HepG2 cells, LPS reduced mitochondrial membrane potential and cellular ATP content but did not modify basal respiration. Stimulated complex II respiration was reduced time-dependently using 1 μg/mL LPS. In primary human hepatocytes, stimulated mitochondrial complex II respiration was reduced time-dependently using 1 μg/mL LPS. In isolated porcine skeletal muscle mitochondria, stimulated respiration decreased at high doses (50 and 100 μg/mL LPS). CONCLUSION LPS reduced cellular ATP content of HepG2 cells, most likely as a result of the induced decrease in membrane potential. LPS decreased cellular and isolated mitochondrial respiration in a time-dependent, dose-dependent and complex-dependent manner.