Tetralin hydrogenation was chosen as a model reaction for aromatics reduction reaction. The effects of sulfur-poisoning on the catalytic properties of gamma-alumina-supported Pt catalysts were investigated by kinetic studies carried out in a continuous fixed-bed reactor at 543 K, under 32 atm total pressure, and weight hourly space velocity (WHSV) ranging from 2.0 to 12 h(-1). An empirical power-law rate reaction was used to model the reaction kinetics. Parameter estimation results indicated that both the reaction order and rate constant decreased with increasing sulfur concentration; 500 ppm sulfur-poisoned catalysts were reactivated by hydrogen treatment at 723 and 823 K, respectively. The electronic properties of fresh, sulfur-poisoned, and hydrogen-reactivated catalysts were investigated by fast Fourier transform infrared (FT-IR) spectroscopy characterizing CO adsorbed on the catalysts. The results indicated that the bond strength between CO and platinum was weakened with the increase of sulfur-poisoning, suggesting that the adsorption of H2S and/or the formation of PtS decreased electronic density of Pt clusters. The electronic density can be regained by hydrogen reactivation, indicated by the results of FT-IR and X-ray absorption near-edge structures (XANES) spectroscopy. The decrease of reaction order with the severity of sulfur-poisoning may have resulted from the decrease of electronic density of the Pt clusters and thus can be recovered with hydrogen reactivation. In contrast, the activity of the sulfur-poisoned catalyst was not fully recovered because of the sulfur-poisoning induced Pt agglomeration and the residue sulfur deposited on Pt sites, inferred from the EXAFS, FT-IR, and chemical analysis results. The comparison of the structure between the sulfur-poisoned and the hydrogen-reactivated catalysts indicates that the adsorbed H2S was removed at 723 K, while the morphology of the Pt clusters had no significant changes after the hydrogen treatment; hydrogen reactivation is unable to redisperse the catalysts.