Glucocorticoid and mineralocorticoid hormones depress liver delta 5 desaturase activity through different mechanisms.

The effects of 11-deoxycorticosterone and aldosterone on liver delta 5 desaturase activity were examined. Both steroid hormones significantly depressed the conversion of [1-14C] eicosatrienoic acid to arachidonic acid. However, the mechanism of action of each of these hormones was different. The effect of 11-deoxycorticosterone was mediated by a soluble protein present in the liver cytosolic fraction. The biological activity of this protein, having a molecular weight lower than 25 kDa, was impaired by trypsin digestion. To determine whether the inhibitory protein was induced through glucocorticoid or mineralocorticoid receptor occupancy, cultured Morris minimal deviation hepatoma cells were pre-treated with the antiglucocorticoid cortexolone or the mineralocorticoid receptor antagonist spironolactone. The results obtained demonstrated that only glucocorticoid receptor structures were involved in the induction of this regulatory protein. The inhibitory response evoked by aldosterone was mediated by a different mechanism. In the case of aldosterone, the inhibitory action affected the microsomal membranes and was not mediated by a soluble protein messenger.