Tamoxifen stimulates arachidonic acid release from rat liver cells by an estrogen receptor-independent, non-genomic mechanism.
BACKGROUND
Tamoxifen is widely prescribed for the treatment of breast cancer. Its success has been attributed to the modulation of the estrogen receptor. I have previously proposed that the release of arachidonic acid from cells may also mediate cancer prevention.


METHODS
Rat liver cells were radiolabelled with arachidonic acid. The release of [3H] arachidonic acid after various times of incubation of the cells with tamoxifen was measured.


RESULTS
Tamoxifen, at micromolar concentrations, stimulates arachidonic acid release. The stimulation is rapid and is not affected by pre-incubation of the cells with actinomycin or the estrogen antagonist ICI-182,780.


CONCLUSIONS
The stimulation of AA release by tamoxifen is not mediated by estrogen receptor occupancy and is non-genomic.
D000818:Animals; D016718:Arachidonic Acid / Q000378:metabolism*; D003470:Culture Media; D004305:Dose-Response Relationship, Drug; D005260:Female; D022781:Hepatocytes / Q000187:drug effects* / Q000378:metabolism; D051381:Rats; D020845:Selective Estrogen Receptor Modulators / Q000494:pharmacology*; D013629:Tamoxifen / Q000494:pharmacology*
D003470:Culture Media; D020845:Selective Estrogen Receptor Modulators; D013629:Tamoxifen; D016718:Arachidonic Acid