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, oestrone and oestradiol-17 beta enhanced the LPS-induced increase in PUT and N1-acetyl-SPD in a dose-dependent manner. Oestradiol-17 alpha and 16 beta-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 alpha-hydroxy-oestradiol (oestriol), 16 alpha-hydroxyestrone, 2-hydroxyoestradiol, 2-hydroxyoesterone, progesterone, testosterone, diethylstilboestrol and nonsteroidal antioestrogens such as tamoxifen and nafoxidine had no effect on the increase. Oestradiol-17 beta enhanced and corticosterone had little effect 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.
Sugimoto
H
H
Department of Physiology, Gumma University, Maebashi, Japan.
Hamana
K
K
Masxuzaki
S
S
Arai
T
T
Yamada
S
S
D000818:Animals; D002251:Carbon Tetrachloride / Q000494:pharmacology; D003345:Corticosterone / Q000494:pharmacology; D003907:Dexamethasone / Q000494:pharmacology; D004958:Estradiol / Q000031:analogs & derivatives / Q000494:pharmacology; D004967:Estrogens / Q000494:pharmacology*; D004970:Estrone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology*; D006854:Hydrocortisone / Q000494:pharmacology; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008099:Liver / Q000187:drug effects / Q000378:metabolism*; D008297:Male; D051379:Mice; D011700:Putrescine / Q000378:metabolism*; D012475:Salmonella; D013095:Spermidine / Q000031:analogs & derivatives* / Q000378:metabolism
D004967:Estrogens; D005938:Glucocorticoids; D008070:Lipopolysaccharides; C017988:N(1)-acetylspermidine; D004970:Estrone; D004958:Estradiol; C021297:16 beta-ethylestradiol-17 beta; D003907:Dexamethasone; D002251:Carbon Tetrachloride; D013095:Spermidine; D011700:Putrescine; D003345:Corticosterone; D006854:Hydrocortisone