Catabolic inactivation

The catabolic inactivation of ABA would be achieved in a stepwise manner. The biological activity of 8 -hydroxy-ABA cannot be tested due to its instability, but several studies have suggested that the activity of 8 -hydroxy-ABA is about 20% of that of ABA.626 683 684 The activity of phaseic acid is low, about 5% of that of ABA, in many biological assays,548 and may be contributed by 8 -hydroxy-ABA present in a sample of phaseic acid. Dihydrophaseic acid and its epimer are almost inactive in assays tested, meaning that the catabolic inactivation is completed in the step reducing phaseic acid to dihydrophaseic acid and its epimer. 

ABSTRACT More than 100 abscisic acid (ABA) analogs have been reported so far. Some were synthesized to clarify structure-activity relationships, and others were developed as tools for investigating the molecular mechanism of ABA action. These analogs, especially those that can be useful tools for studying ABA reception and catabolic inactivation, are summarized together with their design concepts, structural properties and bioactivities. 

The catabolic inactivation of ABA in plants is initiated by hydroxylation at C-8 to produce 8 -hydroxyabscisic acid [8 -HOABA (24)]. 8 -... 

At present resistance to these antibiotics in the screened mutant bacteria appears to be linked to modifications in the permeability of the cell-membrane, or to catabolic inactivation of the drug. 

HA turnover is rapid in the brain, with a half-life of about 30 min. This can change very quickly depending on neuronal activity. There is no high-affinity uptake system for HA once released, HA is inactivated by catabolism. In the brain, released HA is methylated almost exclusively by the enzyme histamine-N-methyltransferase (E.C. 2.1.1.8). The tele-methyl-HA is subsequently degraded by monoamine oxidase-B (MAO-B) and aldehyde dehydrogenase to produce tele-methylimidazoleacetic acid (Brown et ah, 2001). 

Finally, some neurotransmitters, like acetylcholine, are inactivated solely by a catabolic enzyme. Acetylcholinesterase rapidly breaks down the neurotransmitter to acetate and choline, and the choline is then actively transported into the presynaptic... 

Catabolism The breakdown of complex molecules to simpler ones to yield energy (e.g., triacylglycerols to fatty acids) and the inactivation of physiologically active molecules (e.g., acetylcholine to choline and acetic acid). 

The process of oxidative deamination is the most important mechanism whereby all monoamines are inactivated (i.e. the catecholamines, 5-HT and the numerous trace amines such as phenylethylamine and tryptamine). Monoamine oxidase occurs in virtually all tissues, where it appears to be bound to the outer mitochondrial membrane. Whereas there are several specific and therapeutically useful monoamine oxidase inhibitors, inhibitors of catechol-O-methyltransferase have found little application. This is mainly due to the fact that at most only 10% of the monoamines released from the nerve terminal are catabolized by this enzyme. The main pathways involved in the catabolism of the catecholamines are shown in Figure 2.16. 

However, like TOL, TOM encodes the meta-fission of the resulting catechol (Figure 11.4). Consequently, it is unproductive in the assimilation of chloroaromatics like chlorobenzene and 2-chlorophenol, which are also metabolized to 3-chlorocatechol because of catechol 2,3-dioxygenase inactivation. To avoid a build-up of this product an ortho-cleavage enzyme and downstream enzymes for the complete catabolism of the product were recruited through the introduction of the 2,4-dichlorophenoxyacetic-acid-degradativeplasmid pROlOl (Kaphammer, Kukor Olsen, 1990). 

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