Glucocorticoids suppress and oestrogens enhance the lipopolysaccharide-induced increase in putrescine and N1-acetylspermidine in mouse liver

Previously we reported that administration of lipopolysaccharide (LPS) to mice increased the hepatic levels of putrescine (PUT) and N¹-acetylspermidine (N¹-acetyl-SPD). In the current study, we examined the in vivo effects of some steroid hormones on the LPS-induced increase in PUT and N¹-acetyl-SPD. Corticosterone, hydrocortisone and dexamethasone suppressed the LPS-induced increase in PUT and N¹-acetyl-SPD in mouse liver in a dose-dependent manner, dexamethasone being the most effective among them. On the other hand, oesterone and oestradiol-17β enhanced the LPS-induced increase in PUT and N¹-acetyl-SPD in a dose-dependent manner. Oestradiol-17 and 16β-ethyl-oestradiol, as an inactive oestradiol isomer and an antioestrogen, respectively, likewise enhanced the increase in PUT and N¹-acetyl-SPD concentrations induced by LPS. 16-hydroxy-oestradiol (oestriol), 16-hydroxyestrone, 2-hydroxyoestradiol, 2-hydroxyoestrone, progesterone, testosterone, diethylstilboestrol and nonsteroidal antioestrogen such as tamoxifen and nafoxidine had no effect on the increase. Oestradiol-17β enhanced and corticosterone had little on the carbon tetrachloride-induced increase in PUT and N¹-acetyl-SPD. These results suggest that glucocorticoids suppress the increase by preventing the immunological injury by Kupffer cells on hepatocytes and that the stimulatory effect of oestrogens may not be associated with their oestrogenic activities mediated by the oestrogen receptor system.