Stress factor control

The extent to which a particular combination of such "operating environment" factors will be perceived by the workers as being stressful will depend on the available resources such as the quality of the control panel, procedures, training, organizational and social factors, and, finally, the individual characteristics of the workers. The outcome of this transaction between stress factors and coping resources will influence the onset of worker stress. Situations are not stressful merely because of the presence of a number of external stressors, but because they are perceived as such by workers. 

It transpires that the heat shock genes of one single bacterial species are regulated by different mechanisms. Genes and operons controlled by one particular regulator are called regulons and, if there are at least two regulons in one species induced by the same stress factor, they form a stimulon. 

Another example of the coordinated use of herbicides and allelopathic residues is the situation where a herbicide is used to desiccate a cover crop, Lehle and Putnam (131) recognized that the allelochemical content of a residue, such as sorghum, was dependent on the stage of growth at the time of desiccation. However, no studies have been undertaken on other factors that may control the allelochemical content of the residue. It is possible that the quantity and type of allelochemicals in a cover crop can be manipulated by adjusting the formulation and application rate of the herbicides used for desiccation. Evidence in the literature demonstrates that certain herbicide treatments and other stress factors can result in elevations of several coumarins and phenolic compounds (14-19,21). Thus, it may be reasonable to assume that a herbicide used to kill a cover crop can also be used as a stimulus for the synthesis of allelochemicals prior to senescence. 

Fig. 2.8. Factors controlling the production of free radicals in cells and tissues (Rice-Gvans, 1990a). Free radicals may be generated in cells and tissues through increased radical input mediated by the disruption of internal processes or by external influences, or as a consequence of decreased protective capacity. Increased radical input may arise through excessive leukocyte activation, disrupted mitochondrial electron transport or altered arachidonic acid metabolism. Delocalization or redistribution of transition metal ion complexes may also induce oxidative stress, for example, microbleeding in the brain, in the eye, in the rheumatoid joint. In addition, reduced activities or levels of protectant enzymes, destruction or suppressed production of nucleotide coenzymes, reduced levels of antioxidants, abnormal glutathione metabolism, or leakage of antioxidants through damaged membranes, can all contribute to oxidative stress.

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