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On the other hand, 250500 mg/die and short-term therapies are prescribed in ER -independent conditions, such as microbial infections or other ER-negative oncological or fibrotic diseases ( FIGURE 1 Antiproliferative and Oxidative Stress Responses Cell toxicity induced by high tamoxifen concentrations was originally observed in epithelial cells and associated with inhibition of cell proliferation and induction of apoptosis by estrogen-independent mechanisms, later extended also to non-epithelial cells, such as hepatocytes, fibroblasts and retinal cells ( -negative cancers, as well as in infections, envisioning a direct pathogen-killing effect of the drug, and fibrosis, for tamoxifen inhibitory effect on proliferation and activity of renal and peritoneal fibroblasts ( The mechanism of action of tamoxifen cytotoxicity when used at concentrations above the nanomolar range has been linked to the induction of oxidative stress, through the engagement of ER -unrelated, undefined mediators that activate oxidative enzymes or modulate Ca 2+ homeostasis, increasing the intracellular levels of reactive oxygen species (ROS) or oxidized molecules ( The Antimicrobial Activity of Tamoxifen Tamoxifen is effective against a broad range of life-threatening infections

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