Ab initio study of the mechanism of carboxylic acids cross-ketonization on monoclinic zirconia via condensation to beta-keto acids followed by decarboxylation

Catalytic mechanism of acetic and isobutyric acids mixture conversion into two symmetrical and one cross-ketone product on monoclinic zirconia (111) surface was extensively modeled by Density Functional Theory for periodic structures. Several options were evaluated for each mechanistic step by calculating their reaction rate constants. The best option for each kinetically relevant step was chosen by matching calculated rates of reaction with experimental values. Four zirconium surface atoms define each catalytic site. The most favorable pathway includes condensation between surface carboxylates, one of which is enolized through alpha-hydrogen abstraction by lattice oxygen. Condensation of gas phase molecules with the enolized carboxylate on surface is less attainable. The kinetic scheme considers all steps being reversible, except for decarboxylation. The equilibrium constant of the enolization step and the rate constant of the condensation step define the global reaction rate for non-bulky acetic acid. For bulky isobutyric acid, decarboxylation step is added to the kinetic scheme as kinetically significant, while hydrocarbonate departure may also compete with the decarboxylation. Electronic and steric effect of alkyl substituents on the decarboxylation step is disclosed. The cross-selectivity is controlled by both condensation and decarboxylation steps. None of the mechanistic steps require metal oxide to be reducible/oxidizable

Ab initio study of the mechanism of carboxylic acids cross-ketonization on monoclinic zirconia via condensation to beta-keto acids followed by decarboxylation

Catalytic mechanism of acetic and isobutyric acids mixture conversion into two symmetrical and one cross-ketone product on monoclinic zirconia (111) surface was extensively modeled by Density Functional Theory for periodic structures. Several options were evaluated for each mechanistic step by calculating their reaction rate constants. The best option for each kinetically relevant step was chosen by matching calculated rates of reaction with experimental values. Four zirconium surface atoms define each catalytic site. The most favorable pathway includes condensation between surface carboxylates, one of which is enolized through alpha-hydrogen abstraction by lattice oxygen. Condensation of gas phase molecules with the enolized carboxylate on surface is less attainable. The kinetic scheme considers all steps being reversible, except for decarboxylation. The equilibrium constant of the enolization step and the rate constant of the condensation step define the global reaction rate for non-bulky acetic acid. For bulky isobutyric acid, decarboxylation step is added to the kinetic scheme as kinetically significant, while hydrocarbonate departure may also compete with the decarboxylation. Electronic and steric effect of alkyl substituents on the decarboxylation step is disclosed. The cross-selectivity is controlled by both condensation and decarboxylation steps. None of the mechanistic steps require metal oxide to be reducible/oxidizable

m1A and m1G disrupt A-RNA structure through the intrinsic instability of Hoogsteen base pairs

The B-DNA double helix can dynamically accommodate G–C and A–T base pairs in either Watson-Crick or Hoogsteen configurations. Here, we show that G–C(+) and A–U Hoogsteen base pairs are strongly disfavored in A-RNA. As a result, N(1)-methyl adenosine and N(1)-methyl guanosine, which occur in DNA as a form of alkylation damage, and in RNA as a posttranscriptional modification, have dramatically different consequences. They create G–C(+) and A–U Hoogsteen base pairs in duplex DNA that maintain the structural integrity of the double helix, but block base pairing all together and induce local duplex melting in RNA, providing a mechanism for potently disrupting RNA structure through posttranscriptional modifications. The markedly different propensities to form Hoogsteen base pairs in B-DNA and A-RNA may help meet the opposing requirements of maintaining genome stability on one hand, and dynamically modulating the structure of the epitranscriptome on the other