Preparation of Styrenated Phenol by Alkylation of Phenol with Styrene Over SO4²â» /ZrO2 Catalyst.

Styrenated phenols are usually synthesized by the reaction of styrene and phenol under acid catalysts. Styrenated phenol involving high content of di-styrenated phenol (DSP) was synthesized, which can be used to prepare styrenated phenol alkoxylate. The solid catalyst used in this study was prepared by impregnation method. SO4 2- on SO4 2-/ZrO2 catalyst was introduced from an aqueous 1M-H2SO4 solution. The catalysts were characterized by SEM images, XRD patterns, and FT-IR spectra. The catalytic activity was examined by measuring the conversion of phenol and styrene in a liquid-phase batch reactor. Almost 100% conversion of both phenol and styrene over 15-SO4 2-/ZrO2 catalyst were obtained at reaction temperature of 100 °C and reaction time of 6 hr. Amount of catalyst to the reactants was 15 wt%. At same reaction conditions, selectivity of MSP, DSP, and TSP were 23.6%, 52.1%, and 5.4%, respectively. It was known that the selectivity to DSP was increased as IR absorption peak of 1236 cm-1 corresponding to O­S­O bonds was increased.

The Shu complex prevents mutagenesis and cytotoxicity of single-strand specific alkylation lesions.

Three-methyl cytosine (3meC) are toxic DNA lesions, blocking base pairing. Bacteria and humans express members of the AlkB enzymes family, which directly remove 3meC. However, other organisms, including budding yeast, lack this class of enzymes. It remains an unanswered evolutionary question as to how yeast repairs 3meC, particularly in single-stranded DNA. The yeast Shu complex, a conserved homologous recombination factor, aids in preventing replication-associated mutagenesis from DNA base damaging agents such as methyl methanesulfonate (MMS). We found that MMS-treated Shu complex-deficient cells exhibit a genome-wide increase in A:T and G:C substitutions mutations. The G:C substitutions displayed transcriptional and replicational asymmetries consistent with mutations resulting from 3meC. Ectopic expression of a human AlkB homolog in Shu-deficient yeast rescues MMS-induced growth defects and increased mutagenesis. Thus, our work identifies a novel homologous recombination-based mechanism mediated by the Shu complex for coping with alkylation adducts.