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Resistance mechanisms inhibition

Selective toxicity is also important in relation to the development of resistance or tolerance to pollutants from two distinct points of view. On the one hand, there is interest among scientists concerned with crop protection and disease control in mechanisms by which crop pests, vectors of disease, plant pathogens, and weeds develop resistance to pesticides. Understanding the mechanism should point to ways of overcoming resistance, for example, other compounds not affected by resistance mechanisms or synergists to inhibit enzymes that provide a resistance mechanism. On the other hand, the development of resistance can be a useful indication of the environmental impact of pollutants. [Pg.61]

There is evidence that protease inhibitors selectively regulate the activity of specific digestive enzymes at the level of gene expression (Rosewicz et al., 1989). Specifically, soybean trypsin inhibitor increases secretion of proteases, including a form of trypsin that is resistant to inhibition but does not cause an increase in amylase secretion. Although the relationships between protease inhibitors and exocrine pancreatic secretion have received the most attention, pancreatic secretion is increased when potato fiber is added to the diet (Jacob et al., 2000), although the mechanism and signaling pathway have not been elucidated. [Pg.166]

B. Overproduction (A) of PABA is one of the resistance mechanisms of sulfonamides. Changes in the synthesis of DNA gyrases (B) is a well-described mechanism for quinolone resistance. Plasmid-mediated resistance (C) does not occur with quinolones. An active efflux system for transport of drug out of the cell has been described for quinolone resistance, but it is not plasmid mediated. Inhibition of structural blocks (D) in bacterial cell wall synthesis is a basic mechanism of action of p-lactam antibiotics. Inhibition of folic acid synthesis (E) by blocking different steps is the basic mechanism of action of sulfonamides. [Pg.524]

Mechanism of Action An adrenergic agonist that stimulates betaj-adrenergic receptors, resulting in relaxation of uterine and bronchial smooth muscle. Therapeutic Effect Relieves bronchospasm and reduces airway resistance. Also inhibits uterine contractions. [Pg.1186]

The behavior of Insects In selecting a host plant for food and shelter is affected by a wide array of physical and chemical stimuli. Chemicals that play a role in resistance mechanisms may interfere with an Insect s orientation, inhibit feeding, or deter ovipositlon. Most of the known mechanisms of resistance involve feeding deterrents, but the most vulnerable phase of the Insect life cycle may prove to be ovipositlon. Environmental factors may influence the ability... [Pg.209]

Reduction of active uptake in the cell cadmium resistance of Euglena gracilis strains was suggested to be the result of a membrane transport mechanism (inhibition of the membrane cadmium ion transport or increase of the cadmium exclusion mechanism Bariaud et al., 1985). [Pg.166]

In conclusion, the activity of FQ is due to more than one route (Fig. 31). Due to its physicochemical properties, FQ could specifically target the lipid site of hemozoin formation. Its mechanism of action should be in part similar to that of CQ, based on the inhibition of hemozoin formation. Upon the specific (acidic and oxidizing) DV conditions, production of radical oxygen species (ROS) by FQ should be sufficient to promote significant damage on membranes of the parasite DV. The strong activity of FQ on CQ-resistant clones and isolates of P. falciparum suggests a fundamental difference in interaction with resistance mechanisms of the parasite. [Pg.187]

They act as antipathogenic agents and thus affect the process of pathogenesis. They may act on the host through the Induction of plant resistance mechanisms such as stimulation of lignification or enhancement of phytoalexin production. (Please refer to the chapter by Salt and Kuc in this volume for further discussion of this type of compound.) They may act on the pathogen to accentuate elicitor release or to prevent infection (host penetration), colonization (inhibition of phytotoxin synthesis, extracellular enzyme production and action, or phytoalexin degradation) or reproduction. [Pg.40]


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