PMID- 24368668
OWN - NLM
STAT- MEDLINE
DCOM- 20140530
LR  - 20211021
IS  - 1522-1555 (Electronic)
IS  - 0193-1849 (Print)
IS  - 0193-1849 (Linking)
VI  - 306
IP  - 7
DP  - 2014 Apr 1
TI  - Nongenomic effects of estrogen mediate the dose-related myocardial oxidative 
      stress and dysfunction caused by acute ethanol in female rats.
PG  - E740-7
LID - 10.1152/ajpendo.00465.2013 [doi]
AB  - Acute ethanol lowers blood pressure (BP) and cardiac output in proestrus and 
      after chronic estrogen (E2) replacement in ovariectomized (OVX) female rats. 
      However, whether rapid nongenomic effects of estrogen mediate these hemodynamic 
      effects of ethanol remains unanswered. To test this hypothesis, we investigated 
      the effect of ethanol (0.5 or 1.5 g/kg iv) on left ventricular (LV) function and 
      oxidative markers in OVX rats pretreated 30 min earlier with 1 mug/kg E2 (OVXE2) 
      or vehicle (OVX) and in proestrus sham-operated (SO) rats. In SO rats, ethanol 
      caused significant and dose-related reductions in BP, rate of rise in LV pressure 
      (LV dP/dtmax), and LV developed pressure (LVDP). These effects of ethanol 
      disappeared in OVX rats and were restored in OVXE2 rats, suggesting rapid 
      estrogen receptor signaling mediates the detrimental effects of ethanol on LV 
      function. Ex vivo studies revealed that the estrogen-dependent myocardial 
      dysfunction caused by ethanol was coupled with higher LV 1) generation of 
      reactive oxygen species (ROS), 2) expression of malondialdehyde and 
      4-hydroxynonenal protein adducts, 3) phosphorylation of protein kinase B (Akt) 
      and extracellular signal-regulated kinases (ERK1/2), and 4) catalase activity. 
      ERK1/2 inhibition by PD-98059 (1 mg/kg iv) abrogated the myocardial dysfunction, 
      hypotension, and the elevation in myocardial ROS generation caused by ethanol. We 
      conclude that rapid estrogen receptor signaling is implicated in cellular events 
      that lead to the generation of aldehyde protein adducts and Akt/ERK1/2 
      phosphorylation, which ultimately mediate the estrogen-dependent LV oxidative 
      stress and dysfunction caused by ethanol in female rats.
FAU - El-Mas, Mahmoud M
AU  - El-Mas MM
AD  - Department of Pharmacology, School of Medicine, East Carolina University, 
      Greenville, North Carolina.
FAU - Abdel-Rahman, Abdel A
AU  - Abdel-Rahman AA
LA  - eng
GR  - R01 AA014441/AA/NIAAA NIH HHS/United States
GR  - 2R01 AA014441-07/AA/NIAAA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
DEP - 20131224
PL  - United States
TA  - Am J Physiol Endocrinol Metab
JT  - American journal of physiology. Endocrinology and metabolism
JID - 100901226
RN  - 0 (Estrogens)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Animals
MH  - Blood Pressure/drug effects
MH  - Dose-Response Relationship, Drug
MH  - Estrogens/*pharmacology
MH  - Ethanol/*pharmacology
MH  - Female
MH  - Genome/drug effects
MH  - Heart/*drug effects
MH  - Myocardium/*metabolism
MH  - Oxidative Stress/*drug effects
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Time Factors
MH  - Ventricular Dysfunction, Left/*chemically induced/metabolism
PMC - PMC3962612
OTO - NOTNLM
OT  - LV dysfunction
OT  - estrogen
OT  - ethanol
OT  - extracellular signal-regulated kinases
OT  - oxidative stress
EDAT- 2013/12/26 06:00
MHDA- 2014/05/31 06:00
PMCR- 2015/04/01
CRDT- 2013/12/26 06:00
PHST- 2013/12/26 06:00 [entrez]
PHST- 2013/12/26 06:00 [pubmed]
PHST- 2014/05/31 06:00 [medline]
PHST- 2015/04/01 00:00 [pmc-release]
AID - ajpendo.00465.2013 [pii]
AID - E-00465-2013 [pii]
AID - 10.1152/ajpendo.00465.2013 [doi]
PST - ppublish
SO  - Am J Physiol Endocrinol Metab. 2014 Apr 1;306(7):E740-7. doi: 
      10.1152/ajpendo.00465.2013. Epub 2013 Dec 24.