Universidade Federal de Santa Maria

About: Universidade Federal de Santa Maria is a education organization based out in Santa Maria, Brazil. It is known for research contribution in the topics: Population & Context (language use). The organization has 21178 authors who have published 35632 publications receiving 371665 citations.

Preparation of activated carbon from peanut shell by conventional pyrolysis and microwave irradiation-pyrolysis to remove organic dyes from aqueous solutions

Abstract: Activated carbon samples were prepared from peanut shell by conventional pyrolysis (P sample) and microwave irradiation followed by pyrolysis (MW-P sample). These samples as well as peanut shell were characterized by N2 adsorption/desorption isotherms (BET), Fourier transform infrared spectroscopy (FTIR) and scanning electron microscopy (SEM), being applied to remove Direct Black 38 (DB38) and Reactive Red 141 (RR141) dyes from aqueous solutions. In order to evaluate the performance of adsorption process, pH effect, kinetic, equilibrium and desorption studies were carried out in this work. It was found that the MW-P sample exhibited superior characteristics such as texture, surface area, pore volume and pore size than the peanut shell and P sample. In addition, MW-P presented higher values of adsorption capacity, mainly at pH 2.5. The pseudo-second order kinetic model was suitable to represent the adsorption of DB38 and RR141 dyes on the MW-P sample. The Sips isotherm model was adequate to represent the adsorption of DB38 and RR141 on the MW-P sample, being the maximum adsorption capacities of 110.6 and 284.5 mg g−1, respectively. The dyes were desorbed from MW-P sample using an alkaline solution. The results demonstrated that the microwave irradiation followed by pyrolysis is an alternative way to prepare an activated carbon with interesting characteristics and high adsorption capacities for organic dyes.

Diphenyl diselenide and diphenyl ditelluride differentially affect δ‐aminolevulinate dehydratase from liver, kidney, and brain of mice

Abstract: In the present study, the inhibitory effect of diphenyl diselenide and diphenyl ditelluride after in vitro, acute (a single dose), or chronic exposure (14 doses) was examined in mice 24 hours after the last administration. In vitro, diphenyl diselenide, and diphenyl ditelluride inhibited δ-aminolevulinate dehydratase (δ-ALA-D) from brain, liver, and kidney with a similar potency (IC50 5–10 μM), and at 120 μM, they increased the rate of dithiothreitol (DTT) and reduced glutathione (GSH) oxidation. After a single dose (sc), diphenyl diselenide (1 mmol/kg) inhibited the liver (22%, p < 0.01) and brain (27%, p < 0.01) δ-ALA-D, but it did not inhibit the kidney enzyme. After a single dose (sc), diphenyl ditelluride (0.5 mmol/kg) inhibited liver (46%, p < 0.01), kidney (21%, p < 0.05), and brain (39%, p < 0.01) δ-ALA-D. Chronic exposure to diphenyl diselenide (0.125 and 0.250 mmol/kg) caused significant (p < 0.05) increase in liver and liver-to-body weight ratio and inhibited liver (40 and 60%, respectively) and brain (21 and 40%, respectively) δ-ALA-D. Kidney δ-ALA-D was not inhibited significantly after exposure to diphenyl diselenide. Total nonprotein −SH concentration was decreased only in liver of animals exposed for 14 days to selenide. Chronic exposure to diphenyl ditelluride (0.010 and 0.025 mmol/kg) caused significant (p < 0.05) inhibition of liver (28 and 42%, respectively) and brain (23 and 54%, respectively) δ-ALA-D. Kidney δ-ALA-D was not inhibited significantly by diphenyl ditelluride. Total nonprotein −SH concentration was decreased to a different extent after acute or chronic treatment with diphenyl ditelluride depending on analyzed tissue. Hemoglobin content was decreased significantly by 17 and 22% after chronic treatment with 0.125 and 0.25 mmol/kg diphenyl diselenide, respectively. Chronic exposure to 0.010 mmol/kg diphenyl ditelluride caused a reduction of 17% in hemoglobin content that tended to be significant (p < 0.10). These results suggest that δ-ALA-D inhibition after exposure to organochalcogens may perturb heme-dependent metabolic pathway and contribute to the toxicological properties of these compounds. © 2000 John Wiley & Sons, Inc. J Biochem Mol Toxicol 14:310–319, 2000