Estrogen administration attenuates bladder outlet obstruction induced oxidative stress in the female rabbit.
OBJECTIVE
Estrogen administration to female rabbits induces a functional hypertrophy of the bladder. The aim of this study was to investigate whether supplementation of estrogen in the female rabbit with partial bladder outlet obstruction (PBOO) would affect the severity of bladder dysfunction.


METHODS
We surgically created PBOO in female New Zealand White rabbits. Group 1 included sham operated rabbits which served as controls. Group 2 received PBOO without estrogen treatment. Group 3 received estrogen treatment after PBOO. Group 4 received estrogen pretreatment before PBOO. The bladders were then removed for contractile, biochemical, and protein expression studies. There were four rabbits per group.


RESULTS
(1) PBOO resulted in significant decreases in the contractile responses to all forms of stimulation (field stimulation [FS], carbachol, KCl, ATP). Both pretreatment and post-treatment with estrogen resulted in significantly increased contractile responses to all forms of stimulation, although the responses were still lower than control. (2) PBOO resulted in a significant decrease in the activity of choline acetyltransferase (ChAT). Both pretreatment and post-treatment with estrogen resulted in significant increases in ChAT activity back toward control levels. (3) PBOO resulted in significant increases in both protein oxidation and nitration; both pretreatment and post-treatment with estrogen significantly reduced oxidation and nitration toward control levels.


CONCLUSIONS
Estrogen pretreatment and post-treatment in the female rabbit ameliorated contractile and biochemical dysfunctions associated with PBOO. This improvement is likely due to reduced oxidative stress. As expected, pretreatment was generally more effective than post-treatment.
Lin
Wei-Yu
WY
Division of Urology, Chang Gung Memorial Hospital, Chia-Yi, Taiwan.
Li
Suning
S
Leggett
Robert
R
Strassner
Jim
J
Sokol
Rebekah
R
Schuler
Catherine
C
Juan
Yung-Shun
YS
Javed
Zeeshan
Z
Kogan
Barry
B
Levin
Robert M
RM
Mannikarottu
Anita
A
D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000008:administration & dosage*; D002217:Carbachol / Q000494:pharmacology; D002795:Choline O-Acetyltransferase / Q000378:metabolism; D018679:Cholinergic Agonists / Q000494:pharmacology; D004195:Disease Models, Animal; D004334:Drug Administration Schedule; D004558:Electric Stimulation; D004958:Estradiol / Q000008:administration & dosage*; D004967:Estrogens / Q000008:administration & dosage*; D005260:Female; D007279:Injections, Subcutaneous; D009119:Muscle Contraction / Q000187:drug effects*; D018384:Oxidative Stress / Q000187:drug effects*; D011189:Potassium Chloride / Q000494:pharmacology; D050050:Protein Carbonylation / Q000187:drug effects; D011817:Rabbits; D013482:Superoxide Dismutase / Q000378:metabolism; D014443:Tyrosine / Q000031:analogs & derivatives / Q000378:metabolism; D001743:Urinary Bladder / Q000187:drug effects* / Q000201:enzymology / Q000503:physiopathology; D001748:Urinary Bladder Neck Obstruction / Q000188:drug therapy* / Q000378:metabolism / Q000503:physiopathology
D000975:Antioxidants; D018679:Cholinergic Agonists; D004967:Estrogens; C002744:3-nitrotyrosine; D014443:Tyrosine; D004958:Estradiol; D011189:Potassium Chloride; D000255:Adenosine Triphosphate; D002217:Carbachol; D013482:Superoxide Dismutase; D002795:Choline O-Acetyltransferase