Effect of acute and chronic administration of progesterone, estrogen, FSH and LH on oxidant and antioxidant parameters in rat gastric tissue.
This study was conducted to investigate whether gastro-protective and gastro-toxic effects of acute and chronic administration of progesterone, estrogen, FSH and LH were related to oxidant and antioxidant parameters. Chronic administration of progesterone at a low dose (1mg/kg), which probably could not stimulate progesterone receptors (PRs), inhibited oxidative stress of FSH in gastric tissue by suppressing FSH. Progesterone (5mg/kg) may have been caused oxidative stress as reflected by PR stimulation. FSH may have decreased antioxidant parameters and increased oxidant parameters via PRs. Chronic administration of low dose of estrogen (1mg/kg) inhibited LH and but could not stimulate alpha-2 adrenergic receptors, which resulted in oxidative stress in gastric tissue. The higher dose of estrogen (5mg/kg), however, could stimulate alpha-2 receptors, exhibited antioxidant activity in acute and chronic administration. While antioxidant activity of estrogen and LH was blocked with yohimbine (an alpha-2 adrenergic receptor blocker), mifepristone prevented the oxidative stress of progesterone and FSH in gastric tissue. It is concluded that low doses of progesterone may inhibit FSH, whereas high doses of estrogen may stimulate alpha-2 receptors, suggesting that LH could have protective and antioxidant hormone effects.
Kumtepe
Yakup
Y
Atatürk University, Faculty of Medicine, Department of Obstetrics and Gynecology, Erzurum, Turkey.
Borekci
Bunyamin
B
Karaca
Mehmet
M
Salman
Suleyman
S
Alp
Hamit Hakan
HH
Suleyman
Halis
H
D000317:Adrenergic alpha-Antagonists / Q000494:pharmacology; D000818:Animals; D004967:Estrogens / Q000378:metabolism / Q000494:pharmacology*; D005260:Female; D005640:Follicle Stimulating Hormone / Q000378:metabolism / Q000494:pharmacology*; D005753:Gastric Mucosa / Q000378:metabolism*; D005978:Glutathione / Q000378:metabolism; D006727:Hormone Antagonists / Q000494:pharmacology; D007986:Luteinizing Hormone / Q000378:metabolism / Q000494:pharmacology*; D008315:Malondialdehyde / Q000378:metabolism; D015735:Mifepristone / Q000494:pharmacology; D018384:Oxidative Stress / Q000187:drug effects; D009195:Peroxidase / Q000378:metabolism; D011374:Progesterone / Q000378:metabolism / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D013270:Stomach / Q000187:drug effects* / Q000201:enzymology; D013482:Superoxide Dismutase / Q000378:metabolism; D015016:Yohimbine / Q000494:pharmacology
D000317:Adrenergic alpha-Antagonists; D004967:Estrogens; D006727:Hormone Antagonists; D015016:Yohimbine; D015735:Mifepristone; D011374:Progesterone; D008315:Malondialdehyde; D007986:Luteinizing Hormone; D005640:Follicle Stimulating Hormone; D009195:Peroxidase; D013482:Superoxide Dismutase; D005978:Glutathione