Formation antioxidative, phenolic compounds

Type III polyketide synthases are particularly relevant to this chapter because they catalyze the formation of phenolic compounds. This group of polyketide synthases consists of CHSs, stilbene synthase (STS), and curcuminoid synthase (CUS), which perform decarboxylative condensations between a starter unit, either p-coumaroyl-CoA 19 or cinnamoyl-CoA 18, and an extender unit, malonyl-CoA 10. CHS, STS, and CUS convert the substrate molecules into flavo-noids (Cg-Cs-Cg), stilbenoids 8 (Cg-C2-Cg), and curcuminoids 9 (Cg-C7-C6), respectively [59]. Stilbenoids 8 and curcuminoids 9 are out of the scope of this chapter but possess medicinal properties as well resveratrol is a well-known stilbenoid 8 associated with longevity, and curcumin is a common curcuminoid 9 that is responsible for the yellow color in turmeric and can be utilized as a natural pigment possessing antioxidant and anti-inflammatory properties [60-63]. For an in-depth treatment of plant polyketide production in microbes, the reader is directed to a recent comprehensive review by Boghigian et al. [64]. 

There are numerous synthetic and natural compounds called antioxidants which regulate or block oxidative reactions by quenching free radicals or by preventing free-radical formation. Vitamins A, C, and E and the mineral selenium are common antioxidants occurring naturally in foods (104,105). A broad range of flavonoid or phenolic compounds have been found to be functional antioxidants in numerous test systems (106—108). The antioxidant properties of tea flavonoids have been characterized using models of chemical and biological oxidation reactions. 

Oxidation of phenols is one of the most important aspects of these compounds to the biologist. Oxidation of phenolic compounds can result in the browning of tissues. Well-known examples are the browning of lfuits after they have been cut. Oxidation can also result in the formation of metabolites that are toxic to animals and plants, and that can account for spoilage of foods in processing. On the other hand, toxic compounds formed from the oxidation of phenolics can inhibit pathogenic microorganisms. Certain phenols are used as retardants or antioxidants to prevent the oxidation of fatty acids. 

Effect of a Phenolic Antioxidant. The rate of decomposition of a solution containing the hydroperoxide (5.0 X 10 2 mole/liter) dilauryl thiodipropionate (2.5 X 10 2 mole/liter) and l,l,3-tris(2 -methyl-5 -fert-butyl-4 -hydroxyphenyl) butane (2.5 X 10"2 mole/liter) at 80°C. was identical with that containing no phenolic compound. In addition no formation of polymer was observed when solutions of Tetralin hydroperoxide and dilauryl thiodipropionate were allowed to react at 70 °C. in sealed tubes in the presence of inhibitor-free acrylonitrile in nitrogen... 

Based on in vitro experiments, the mode of antioxidant action of phenolic compounds has been suggested as involving an electron transfer to the phenolic compound substances with a possible chinon function form a semichinon radical [48, 49]. Further mechanisms/modes of action have been discussed, e.g., the ability of catechin/epicatechin and derivatives to scavenge the tyrosyl radical intermediate involved in ROS-derived nitrotyrosine formation [50]. 

The formation of polymers leads to an increase in viscosity. The various lipids that can leach into the frying oil change the properties and the performance of the frying oil. Colored lipids solubilized in the oil contribute to the darkening. Phospholipids are emulsifiers. Traces of liposoluble metal compounds may act as prooxidants. Liposoluble vitamins and phenolic compounds are antioxidants. Volatile compounds (e.g., from fish or onions) contribute to off-flavors. 

O-tetradecanoylphorbol-13-acetate-induced hydrogen peroxide formation in mouse epidermis, in Phenolic Compounds in Foods andHealth II Antioxidant and Cancer Prevention, Huang, M.T., Ho, C.T., and Lee, C.Y., Eds., Washington, DC, 1992, pp. 308-314. 

Caffeic Acid Phenethyl Ester (CAPE). CAPE, a phenolic compound with antioxidant properties, is an active ingredient derived from honeybee propolis (52). CAPE has antiviral, anti-inflammatory and antiproliferative properties. The compound differentially suppresses the growth of numerous human cancer cells and also inhibits tumor promoter-mediated processes in transformed cells (53,54). In transformed cells, CAPE induces apoptosis and inhibits the expression of the malignant phenotype (55,56). In addition, CAPE treatment attenuates the formation of azoxymethane-induced aberrant crypts and the activities of ornithine decarboxylase (ODC), tyrosin protein kinase, and lipoxygenase activity (57). Although the molecular basis for these multiple chemopreventive effects of CAPE is not clear, recent studies have demonstrated that CAPE is a potent and specific inhibitor of the transcription factor NF-kB (58). CAPE inhibited the activity and expression of COX-2 in the carrageenan air pouch model of inflammation as well as in TPA-treated human oral epithelial cells (59). CAPE was able to reduce neointimal formation by inhibiting NF-kB activation in a model of endothelial injury of rat carotid artery (60). 

These cosolutes are important in the present context since phenolic compounds are commonly included as antimicrobial agents or as antioxidants in aqueous formations which may also contain a water-soluble polymer such as PVP. 

Another line of investigation is bridging polyphenol activity with NO bioavailability via the chemical reduction of nitrite to NO (Takahama et al, 2002 Peri et al, 2005 Gago et al, 2007). The redox properties that have been proposed to confer polyphenols with antioxidant activity by quenching oxidizing radicals may, alternately, endow the phenolic compounds with the capacity to promote the formation of NO from nitrite, particularly in the gastrointestinal tract, a location where both nitrite and polyphenols achieve high concentrations. 

---