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This article deals with the effects of SiO2/Al2O3 ratio of HZSM-5 catalysts in disproportionation and ethylation of ethylbenzene to produce para-diethylbenzene (p-DEB). The physicochemical characterization of the catalyst samples shows that the variation of SiO2/Al2O3 has minimal impact on the crystallinity of HZSM-5 samples. On the other hand, the acidity of the materials decreased while specific surface area increased with increasing the SiO2/Al2O3 ratios. The catalytic experiment in the CREC Riser Simulator shows that low temperature favors the EB ethylation reaction while higher temperature is favorable for disproportionation. The DEB selectivity is found to be significantly higher in ethylation of EB with ethanol than disproportionation. Among the five HZSM-5 catalysts, the sample with SiO2/Al2O3=80 gives highest EB conversion and is more selective to DEB although the p-DEB/m-DEB for the catalysts are comparable with other samples. The value of the activation energy for EB cracking is comparable to the activation energy of EB disproportionation which is consistent to the high benzene selectivity in this route. During the EB ethylation with ethanol, a small amount of benzene was formed via the cracking of EB, which is reflected by higher activation energy of the EB cracking reaction. The kinetics analysis also confirms that during EB ethylation, the disproportionation and cracking of EB is negligible. In EB ethylation, the HZSM-5 catalyst with SiO2/Al2O3=80 requires lowest amount of activation energy to form DEB which is reflected in higher DEB selectivity of the catalyst.

Cultured Chinese hamster ovary cells were treated with ethylating agents. DNA lesions giving rise to single-strand breaks (ssb) or alkali-labile sites were measured by centrifugation in alkaline sucrose gradients after lysis in alkali. 4 agents with different tendencies to ethylate preferentially either at N or O atoms were compared, namely N-ethyl-N'-nitro-N-nitrosoguanidine (ENNG), N-ethyl-N-nitrosourea (ENU), ethyl methanesulphonate (EMS) and diethyl sulphonate (DES). The compounds differed greatly in their potency to induce the lesions measured when compared on a molar basis, but comparison at equicytotoxic doses showed relatively small differences. Upon prolonged incubation of the DNA in alkali, the number of ssb increased considerably. DNA from untreated cells showed biphasic kinetics: slow ssb formation for about 10 h, then the rate increased and remained constant for up to 40 h. Treated cells showed an accelerated, dose-dependent linear generation of ssb for 10 h, followed by a short plateau; then ssb were formed again at a constant rate, somewhat higher than that in controls. Ssb formed in the initial phase are ascribed to phosphotriester hydrolysis, those after the plateau to unidentified causes. Zero intercepts appeared to be a measure of apurinic sites generated intracellularly. A 24-h repair period preceding lysis reduced the ENNG intercept, but not that of DES. Rapid degradation of DES during the 1-h treatment occurred, so most 'apurinic-site lesions' were induced in the beginning of exposure and possibly were already repaired at the end. The types of lesion distinguished (reparable and non-reparable apurinic sites, phosphotriesters) appeared of little consequence for cell survival. Chemicals/CAS: diethyl sulfate, 64-67-5; ethylnitronitrosoguanidine, 4245-77-6; ethylnitrosourea, 759-73-9; mesylic acid ethyl ester, 62-50-0; Alkylating Agents; diethyl sulfate, 64-67-5; DNA, 9007-49-2; ENNG, 4245-77-6; Ethyl Methanesulfonate, 62-50-0; Ethylnitrosourea, 75