Desulfurization of high sulfur petroleum coke by molten caustic leaching

Desulfurization by molten caustic leaching (MCL) at 400–500 °C has been investigated in order to reduce the sulfur content of petroleum coke. Effective parameters on desulfurization of petroleum coke, other than temperature, include alkali to feed (petroleum coke) mass ratio, time and mesh size in the ranges of 0.5–1.5, 1–3 h and 200–600 µm, respectively. In this work, petroleum coke desulfurization conditions using solid KOH have been studied. Maximum petroleum coke desulfurization by MCL method has been obtained by Taguchi L9 design using alkali to feed mass ratio of 1, temperature of 600 °C, time of 2 h and mesh size of 200 µm. The changes in the main groups on the coke surface have been determined using FTIR spectroscopy. In addition, SEM-EDX, TGA and XRD analyses have been used to investigate the changes in coke physical and chemical properties.     

A novel one-pot biosynthesis of pure alpha aluminum oxide nanoparticles using the macroalgae Sargassum ilicifolium: A green marine approach

A novel biological method is proposed for producing ceramic alpha aluminum oxide nanoparticles using an extract of the algae Sargassum ilicifolium. The algal extract functions as a bioreducing as well as a stabilizer agent. The presence of an absorption peak at 227?nm, confirmed the formation of the aluminum oxide nanoparticles using a UV–visible spectroscopy. FTIR analysis indicated that bioreduction of aluminum ions and nanoparticle stabilization probably occurred by interactions between aluminum and the biofunctional groups of algal extract. The XRD pattern revealed that after calcination at ~ 1200?°C, the Al₂O₃ nanoparticles were alpha crystalline in nature with a diameter of 35?nm and had a rhombohedral structure. TEM indicated that the alumina nanoparticles were well-dispersed and spherical in shape with an average size of 20?±?2.1?nm. EDX spectroscopy revealed that the sample contained only aluminum (46.31%) and oxygen (53.69%), confirming the high purity of the alumina nanopowder. The results demonstrated that alpha alumina NPs has an optical band gap of 5.46?eV.     

Toxicological assessment of 3-monochloropropane-1,2-diol (3-MCPD) as a main contaminant of foodstuff in three different in vitro models: Involvement of oxidative stress and cell death signaling pathway

3-Monochloropropane-1,2-diol (3-MCPD) as a main source of food contamination has always been known as a carcinogenic agent. Kidney, liver, testis, and heart seem to be the main target organs for 3-MCPD. Because oxidative stress and mitochondrial dysfunction have been realized to be involved in 3-MCPD-induced cytotoxicity, the present study aimed to investigate the probable toxicity mechanisms of 3-MCPD in isolated mitochondria, HEK-293 cell line, and cell isolated from the rats’ liver and kidney through measuring multiparametric oxidative stress assay. Based on the data indicating no significant difference between 3-MCPD-treated groups and control group, metabolites of 3-MCPD have a key role in organ toxicity caused by them. To further investigating the suggested hypothesis, the effect of 3-MCPD toxicity on HEK-293 cell line was examined. Although the proliferation declined after exposure to a low dose of 3-MCPD (10 to 200 µM), controversial responses in higher concentration (2 to 10 mM) have led to studies on the effect of oxidative stress and cell death signaling on isolated kidney and liver cells. Treatment of the isolated kidney and liver cells with 3-MCPD resulted in an increase in the level of reactive oxygen species (ROS), the collapse of mitochondrial membrane potential (MMP), and activation of cell death signaling without creating any significant difference in the amount of reduced glutathione. In fact, 3-MCPD can disrupt the mitochondrial electron transfer in isolated cells, which is correlated with the impairment of mitochondrial oxidative phosphorylation system, the rise of ROS level, and the failure of MMP, leading to the release of cytochrome c from mitochondria to cytosol and finally the activation of cell death signaling.