Inhibition—acceleration mechanism

The inhibition-acceleration mechanism. Moffat et al. (37) proposed the inhibition-acceleration mechanism to explain the experimentally observed comer rounding (inversion of curvature. Fig. 19 in Ref. 37) and general shape evolution in superconformal electrodeposition of copper in vias and trenches of nanometer dimensions (37,38). These authors also smdied a three-additive system composed of two inhibitors and one accelerator. They concluded that superconformal deposition and comer rounding may be attributed to competitive adsorption of inhibitor and accelerator. This model is based on the assumption of curvature (in vias and trenches) -enhanced accelerator coverage. 

Two mechanisms for super-conformal deposition in the presence of additives have been proposed the differential-inhibition mechanism and the inhibition-acceleration mechanism. 

The second model in this category is based on the inhibition-acceleration mechanism. The basic assumption of tins model is that the accelerator is strongly adsorbed on the surface thereby displacing the inhibitor. 

That the type II deiodinase represents a common enzyme for the ORD of T4 and rT3 is supported by their mutual competitive inhibition with corresponding Km and /C( values [72-74,82,83]. T3, which is not a substrate for the type II deiodinase, also does not inhibit the deiodination of T4 and rT3 in vitro. In addition to competitive substrate inhibition, other mechanisms exist for the regulation of type II enzyme activity by thyroid hormone in vivo. Experimental hypothyroidism in rats induces a large increase in type II activity in the CNS [71,82], pituitary [72,83,87] and BAT [73] at least in part by prolongation of the half-life of the enzyme [88]. Treatment of hypothyroid rats with T3 produces a rapid fall in type II deiodinase in CNS and pituitary which appears to be due to an accelerated inactivation of the enzyme [88]. 

Addition Chlorination. Chlorination of olefins such as ethylene, by the addition of chlorine, is a commercially important process and can be carried out either as a catalytic vapor- or Hquid-phase process (16). The reaction is influenced by light, the walls of the reactor vessel, and inhibitors such as oxygen, and proceeds by a radical-chain mechanism. Ionic addition mechanisms can be maximized and accelerated by the use of a Lewis acid such as ferric chloride, aluminum chloride, antimony pentachloride, or cupric chloride. A typical commercial process for the preparation of 1,2-dichloroethane is the chlorination of ethylene at 40—50°C in the presence of ferric chloride (17). The introduction of 5% air to the chlorine feed prevents unwanted substitution chlorination of the 1,2-dichloroethane to generate by-product l,l,2-trichloroethane. The addition of chlorine to tetrachloroethylene using photochemical conditions has been investigated (18). This chlorination, which is strongly inhibited by oxygen, probably proceeds by a radical-chain mechanism as shown in equations 9—13. 

Heterogeneities associated with a metal have been classified in Table 1.1 as atomic see Fig. 1.1), microscopic (visible under an optical microscope), and macroscopic, and their effects are considered in various sections of the present work. It is relevant to observe, however, that the detailed mechanism of all aspects of corrosion, e.g. the passage of a metallic cation from the lattice to the solution, specific effects of ions and species in solution in accelerating or inhibiting corrosion or causing stress-corrosion cracking, etc. must involve a consideration of the detailed atomic structure of the metal or alloy. 

It hag been shown that transition of a backbone carbon from the sp to sp state is promoted by tensile stresses and inhibited by compressive strains (10,44). The acceleration of the process of ozone oxidation of the polymers under load is not associated with the changes in supramolecular structure or segmental mobility of the chain. The probably reason of this effect is a decreasing of the activation energy for hydrogen abstraction (44). The mechanism of initial stages of the reaction of ozone with PP can be represented as ... 

As noted previously, rate accelerations imposed by the cycloamyloses may be competitively inhibited by the addition of inert reagents to the reaction medium. The inhibitor, by competing with the substrate for the cycloamylose cavity, effectively removes a fraction of the catalyst from the reaction coordinate. This observation lends additional force to the mechanism illustrated in scheme I. 

Thus, the mechanism of MT antioxidant activity might be connected with the possible antioxidant effect of zinc. Zinc is a nontransition metal and therefore, its participation in redox processes is not really expected. The simplest mechanism of zinc antioxidant activity is the competition with transition metal ions capable of initiating free radical-mediated processes. For example, it has recently been shown [342] that zinc inhibited copper- and iron-initiated liposomal peroxidation but had no effect on peroxidative processes initiated by free radicals and peroxynitrite. These findings contradict the earlier results obtained by Coassin et al. [343] who found no inhibitory effects of zinc on microsomal lipid peroxidation in contrast to the inhibitory effects of manganese and cobalt. Yeomans et al. [344] showed that the zinc-histidine complex is able to inhibit copper-induced LDL oxidation, but the antioxidant effect of this complex obviously depended on histidine and not zinc because zinc sulfate was ineffective. We proposed another mode of possible antioxidant effect of zinc [345], It has been found that Zn and Mg aspartates inhibited oxygen radical production by xanthine oxidase, NADPH oxidase, and human blood leukocytes. The antioxidant effect of these salts supposedly was a consequence of the acceleration of spontaneous superoxide dismutation due to increasing medium acidity. 

Although technical chlordane is a mixture of compounds, two metabolites — heptachlor epoxide and oxychlordane — can kill birds when administered through the diet (Blus et al. 1983). These two metabolites originate from biological and physical breakdown of chlordanes in the environment, or from metabolism after ingestion. Heptachlor can result from breakdown of cis- and trans-chlordane, eventually oxidizing to heptachlor epoxide oxychlordane can result from the breakdown of heptachlor, m-chlordane, tra .s-chlordane, or fram-nonachlor (Blus et al. 1983). Heptachlor epoxide has been identified in soil, crops, and aquatic biota, but its presence is usually associated with the use of heptachlor, not technical chlordane — which also contains some heptachlor (NRCC 1975). Various components in technical chlordane may inhibit the formation of heptachlor epoxide or accelerate the decomposition of the epoxide, but the actual mechanisms are unclear (NRCC 1975). 

Fig. 6.2. Proposed mechanisms of action of pure antiestrogens (fulvestrant). 1 Fulvestrant (ICI) binds to estrogen receptor (ER). 2 Fulvestrant binding to ER accelerates receptor degradation ( ER down-regulator ). 3 Rate of dimerization and nuclear localization of fulvestrant-ER complex is reduced. 4 Reduced binding of fulvestrant-ER to ERE. 5 No transcription of estrogen-responsive genes since AF-1 and AF-2 are inactive, no coactivators are recruited and the activity of RNA polymerase II is not activated (or inhibited) (Wakeling 2000)...

These are analogous to the reactions postulated for hydrocarbon systems by Laidler et al.115,176. With certain hydrocarbons there is almost no inhibition region, and the main effect of nitric oxide is to accelerate the rate of decomposition as in the present instance. Further work on this interesting aspect of the decomposition of S2F10 is obviously desirable. In addition, attention should be given to the effects of inert gases on the orders of the individual reactions in the above mechanism, and on the rate of the heterogeneous reaction. 

Mn2+, D.F.P.-ase is further activated by cysteine, histidine, thiolhistidine, and serine, histamine and 2 2 -dipyridyl. Reagents reacting with metal ions, SH groups and carbonyl groups inhibit D.F.P.-ase activity. Work is proceeding on the further elucidation of such mechanisms.1 In a somewhat similar connexion attention is called to the fact that the non-enzymic hydrolysis of D.F.P. is accelerated by heavy metals and their complexes, in particular by copper chelates of ethylene diamine, o-phenanthroline, 2 2 -dipyridyl and histidine.2... 

K. Nakai, S. Tazuma, T. Nishioka and K. Chayama, Inhibition of cholesterol crystallization under bilirubi deconjugation partial characterization of mechanism whereby infected bile accelerates pigment stone formation. Biochem. Biophys. Acta 1632 (2003) 48-54. 

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