Reference

Sulfated SnO2-SiO2 superacid catalysts by sol-gel method

Sulfated SnO2-SiO2 superacid catalysts by sol-gel method. Salas, P.; Hernandez, J.G.; Lopez-Salinas, E.; Schifter, I.; Llanos, M.E.; Navarrete, J.; Morales, J. (Instituto Mexicano del Petroleo, Subdireccion de Transformacion Industrial, Mexico 07730, Mex.). Journal of Porous Materials, 3(4), 241-245 (English) 1996 Kluwer. CODEN: JPMAFX. ISSN: 1380-2224. DOCUMENT TYPE: Journal CA Section: 67 (Catalysis, Reaction Kinetics, and Inorganic Reaction Mechanisms) Section cross-reference(s): 66 A series of sulfated SnO2-SiO2 binary oxides were prepd. by the sol-gel method with different SnO2 molar content. Tin chloride and tetraethylorthosilicate were used as precursors. The resulting solids were characterized by Fourier Transform IR spectroscopy (FTIR), ammonia thermodesorption, surface area measurements and also titrated using Hammett indicators. To correlate the acidic properties with catalytic activity, solids were tested in the 2-propanol decompn. reaction. SnO2 addn. to SiO2 produce a twofold synergetic effect: an increase in the surface area in most of the resulting mixed oxides and high catalytic activities for the dehydration reaction. The titrated materials, using Hammett indicators, are of superacid nature (Ho ￡ - 13.7).Except for chemicals metioned above, 58500-40-6 and 7631-86-9 are also used. .

Tin chloride pretreatment prevents renal injury in rats with ischemic acute renal failure

Tin chloride pretreatment prevents renal injury in rats with ischemic acute renal failure. Toda, Narushi; Takahashi, Toru; Mizobuchi, Satoshi; Fujii, Hiromi; Nakahira, Kiichi; Takahashi, Shuji; Yamashita, Masami; Morita, Kiyoshi; Hirakawa, Masahisa; Akagi, Reiko (Department of Anesthesiology and Resuscitology, Okayama University Medical School, Okayama, Japan). Critical Care Medicine, 30(7), 1512-1522 (English) 2002 Lippincott Williams & Wilkins. CODEN: CCMDC7. ISSN: 0090-3493. DOCUMENT TYPE: Journal CA Section: 1 (Pharmacology) Rats were injected with SnCl2 s.c., because this is known to specifically and potently induce renal heme oxygenase activity. Anesthetized rats were subjected to bilateral flank incisions, and the right kidney was removed. Renal ischemia for 40 min was performed by left renal microvascular clamping, followed by reflow of the blood. SnCl2 treatment specifically induced heme oxygenase-1 mRNA and protein in the proximal tubular epithelial cells of the kidney without apparent cell injury. SnCl2 treatment before renal ischemia augmented the induction of heme oxygenase-1 at both the transcriptional and protein levels in the renal epithelial cells compared with untreated animals. SnCl2 pretreatment, which decreased microsomal heme concn., decreased the ischemic renal injury, as judged by the decrease in serum creatinine and blood urea N concns. and the lesser tubular epithelial cell injuries. In contrast, inhibition of heme oxygenase activity by treatment with tin mesoporphyrin, which increased microsomal heme concn., abolished the beneficial effect of SnCl2 pretreatment. These findings indicate that SnCl2 pretreatment ameliorates renal injury in rats with acute ischemic renal failure by virtue of its specific heme oxygenase-1 induction in renal epithelial cells. The findings also suggest that heme oxygenase-1 induction plays an important role in protecting renal cells from oxidative damage caused by heme.