Estradiol‐17β modifies the induction of spermidine/spermine N1‐acetyltransferase activity in the liver of lipopolysaccharide‐treated mice

ABSTRACT— In an attempt to elucidate the effects of estrogen on polyamine metabolism in lipopolysaccharide (LPS)‐treated mice, we assayed polyamine content and the activity of spermidine/spermine N1‐acetyltransferase (SAT) and ornithine decarboxylase (ODC) in some organs. LPS elevated N'‐acetylspermidine levels in the liver and lung and putrescine levels in the liver, lung and spleen. LPS increased the activity of ODC at 6 h and that of SAT at 12 h in the liver. When estradiol‐17β was simultaneously administered with LPS, the maximum increase in hepatic N1‐acetylspermidine levels was found 6 h earlier than in the LPS control. Likewise, the peak of the hepatic SAT activity after LPS‐treatment was observed 6 h earlier in the estradiol‐17β‐treated mice than in the LPS control. No such effect of estradiol‐17β was found in the lung and spleen. The LPS‐induced ODC activity was not affected by estradiol‐17β in the liver, lung or spleen. Estrone and 16β‐ethylestradiol (an anti‐estrogen) were also effective in enhancing the LPS‐induced elevation of N1‐acetyl‐spermidine and putrescine in the liver, while both diethylstilbestrol, which has a potent estrogenic activity without steroid structure and estradiol‐17α (a non‐estrogenic isomer of estradiol‐17β) were without effect. Tamoxifen (an estrogen receptor antagonist) did not suppress the estrogen‐induced increase in hepatic N1‐acetylspermidine levels.