Resistance involves numerous mechanisms including decreased drug uptake, increased drug efflux along with reduction of intracellular drug concentration, activation of detoxifying systems, activation of altered DNA repair mechanisms, evasion of drug-induced apoptosis, induced emergency response genes to impair apoptotic pathway, etc.
The resistance occurs through multiple mechanisms, including decreasing the cell membrane content of ergosterol.
This association is plausibly supported by several biological mechanisms, including decreased inflammation, decreased insulin-like growth factor levels, reduced hyperinsulinemia and modulated immune function (Wolin et al, 2009).
Numerous mechanisms, including decreased permeability, efflux pump overexpression, and carbapenemase production, can be responsible for the resistance to carbapenems [ 7, 32, 33].
Moreover, this association is plausibly supported by several biological mechanisms, including decreased inflammation, reduced intestinal transit time, decreased insulin-like growth factor levels, reduced hyperinsulinemia and modulated immune function with physical activity.
Detrimental effects of hyperglycaemia-induced increase in polyol pathway flux could be explained by a number of proposed mechanisms including decreased (Na+&K+) ATPase activity, sorbitol-induced osmotic stress, decrease in cytosolic NADPH, and increase in cytosolic NADH/NAD+.
Chemo-resistance can result from numerous mechanisms, including decreased intracellular drug concentrations, an augmented ability to repair DNA damage or endure stress, as well as the prevention of cell death.
Several studies have shown that fibroblasts from IPF patients are resistant to apoptosis, and in particular Fas-mediated apoptosis, through a number of potential mechanisms, including decreased expression of the surface receptor Fas.
23 24 Although several mechanisms, including decreased NO bioavailability, 25 excessive oxidative stress induced by angiotensin II, 26 and inflammation, 27 have been proposed, the pathogenesis of the relation between hypertension and endothelial dysfunction is not fully understood.
Ambrose and Barua (2004) suggest that the underlying mechanisms, including decreases in brachial artery endothelium dependent vasodilation, abnormalities in nitric oxide biosynthesis, and increases in platelet activation, may become saturated at even relatively low doses of cigarette smoke.
