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The nitric acid concentration/sulfuric acid concentration (NAC/SAC) process has been widely used for concentrating dilute aqueous nitric acid and recovering spent sulfuric acid. Dilute nitric acid (65 to 80 wt %) is concentrated using sulfuric acid to bind water and break the nitric acid‐water azeotrope at approximately 68 wt % nitric acid. To support heat and mass balance calculations and process simulation for NAC/SAC processes, we develop a comprehensive thermodynamic model for nitric acid‐sulfuric acid‐water ternary system based on previously published thermodynamic models of nitric acid‐water and sulfuric acid‐water binary systems with eNRTL equation. The ternary system model correlates well the isobaric vapor‐liquid equilibrium data at one atmosphere and the water and nitric acid activities data at 273.15 K for the ternary. Contour plots of boiling points, vapor phase composition, and specific heat capacity of the ternary system, as well as a Merkel enthalpy‐concentration chart are generated for engineering use. © 2017 American Institute of Chemical Engineers AIChE J, 63: 3110–3117, 2017

A BSTRACT Introduction: This study investigated the role of diallyl disulfide (DADS) against glycerol-induced nephrotoxicity in rats. Moreover, the role of peroxisome proliferator activated receptor-γ (PPAR-γ) in DADS-mediated renoprotection has been explored. Materials and Methods: Male Wistar albino rats were challenged with glycerol (50% w/v, 8 mL/kg intramuscular) to induce nephrotoxicity. Kidney injury was quantified by measuring serum creatinine, creatinine clearance, urea, potassium, fractional excretion of sodium, and microproteinuria in rats. Renal oxidative stress was measured in terms of thiobarbituric acid reactive substances, superoxide anion generation, and reduced glutathione levels. Hematoxylin–eosin (H&E) and periodic acid Schiff staining of renal samples was done to show histological changes. Glycerol-induced muscle damage was quantified by assaying creatine kinase (CK) levels in rat serum. Results: Administration of glycerol resulted in muscle damage as reflected by significant rise in CK levels in rats. Glycerol intoxication led kidney damage was reflected by significant change in renal biochemical parameters, renal oxidative stress and histological changes in rat kidneys. Administration of DADS attenuated glycerol-induced renal damage. Notably, pretreatment with bisphenol A diglycidyl ether, a PPAR-γ antagonist, abolished DADS renoprotection in rats. Conclusion: We conclude that DADS affords protection against glycerol-induced renal damage in rats. Moreover, PPAR-γ plays a key role in DADS-mediated renoprotective effect.