Phenols growth inhibition

Essential oils are known to have detrimental effects on plants. The inhibitory components have not been identified, but both alde-hydic (benzol-, citrol-, cinnamal-aldehyde) and phenolic (thymol, carvacol, apiol, safrol) constituents are suspected. Muller et al. (104) demonstrated that volatile toxic materials localized in the leaves of Salvia leucophylla, Salvia apiana, and Arthemisia californica inhibited the root growth of cucumber and oat seedlings. They speculated that in the field, toxic substances from the leaves of these plants might be deposited in dew droplets on adjacent annual plants. In a subsequent paper, Muller and Muller (105) reported that the leaves of S. leucophylla contained several volatile terpenes, and growth inhibition was attributed to camphor and cineole. 

It has been shown that in some compounds the active species is the non-ionized molecule while the ion is inactive (benzoic acid, phenols, nitrophenols, salicylic acid, acetic acid). Thus, conditions of pH which favour the formation of the ions of these compounds will also reduce their activity. The effect of pH on the ability of acetic acid and phenol to inhibit the growth of a mould is shown in Fig. 11.4. 

Scopoletin is purported as the most widely distributed coumarin in higher plants, and scopoletin, umbelliferone, and esculetin are the ones most frequently linked to allelopathy. Given their phenylpropane origin, it is not surprising that these simple coumarins have many actions in common with the cinnamic acids. One variance is that coumarin and scopoletin have been reported to decrease mitosis,2 whereas at least at concentrations that correlate with growth inhibition, the phenolic acids do not appear to affect cell division. 

Bacterial or enzymatic toxicity tests are used to assay the activity of organic compounds including solvents. A survey of environmental bacterial or enzymatic test systems is given by Bitton and Koopman. The principles of these test systems are based on bacterial properties (growth, viability, bioluminescence, etc.) or enzymatic activities and biosynthesis. The toxicity of several solvents were tested in bacterial or enzymatic systems, e.g., pure solvents such as phenol in growth inhibition assays (Aeromonas sp.), solvents in complex compounds such as oil derivates, solvents in environmental samples such as sediments or solvents used in the test systems.The efficiency of several test systems, e.g., Microtox tests or ATP assays, vary, e.g., looking at the effects of solvents. ... 

Another control effect may occur in the metabolic sequence leading from L-tryptophan to lAA. Natural phenolic growth inhibitors were checked for their influence on indole metabolism in the plants from which they were isolated, and were found to change the incorporation pattern of the radioactive precursor (Table 3) Although growth promotion and inhibition by phenols could thus partially be explained by the action of phenols on lAA biosynthesis, an effect on lAA destruction also seems feasible(3). 

The counter effects of phytohormones, like lAA, on phenolic inhibitors are not excluded. Hence, primary growth regulation starts at the level of biosynthesis of growth promoting and growth inhibiting substances. 

Effects of phenolic acids, wheat Triticum aestivum L. Southern States 555 ) or sunflower tissues Helianthus anmus L.) on phenolic acid-utilizing bacteria in the bulk soil and rhizosphere of cucumber seedlings and growth inhibition of cucumber seedlings were determined (Staman et al. 2001) as previously described. Eor details see Section 2.2.11. The effect of sunflower leaf tissue on pigweed seedling emergence was also determined, as described above. 

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