scholarly journals Acute Ethanol Gavage Attenuates Hemorrhage/Resuscitation-Induced Hepatic Oxidative Stress in Rats

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
B. Relja ◽  
K. Wilhelm ◽  
M. Wang ◽  
D. Henrich ◽  
I. Marzi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ethanol Intoxication ◽  
Arterial Blood ◽  
Inos Protein Expression ◽  
Acute Ethanol ◽  
Acute Fatty Liver ◽  
Acute Ethanol Intoxication ◽  
Subsequent Resuscitation

Acute ethanol intoxication increases the production of reactive oxygen species (ROS). Hemorrhagic shock with subsequent resuscitation (H/R) also induces ROS resulting in cellular and hepatic damagein vivo. We examined the role of acute ethanol intoxication upon oxidative stress and subsequent hepatic cell death after H/R. 14 h before H/R, rats were gavaged with single dose of ethanol or saline (5 g/kg, EtOH and ctrl; H/R_EtOH or H/R_ctrl, resp.). Then, rats were hemorrhaged to a mean arterial blood pressure of30±2 mmHg for 60 min and resuscitated. Two control groups underwent surgical procedures without H/R (sham_ctrl and sham_EtOH, resp.). Liver tissues were harvested at 2, 24, and 72 h after resuscitation. EtOH-gavage induced histological picture of acute fatty liver. Hepatic oxidative (4-hydroxynonenal, 4-HNE) and nitrosative (3-nitrotyrosine, 3-NT) stress were significantly reduced in EtOH-gavaged rats compared to controls after H/R. Proapoptotic caspase-8 and Bax expressions were markedly diminished in EtOH-gavaged animals compared with controls 2 h after resuscitation. EtOH-gavage increased antiapoptotic Bcl-2 gene expression compared with controls 2 h after resuscitation. iNOS protein expression increased following H/R but was attenuated in EtOH-gavaged animals after H/R. Taken together, the data suggest that acute EtOH-gavage may attenuate H/R-induced oxidative stress thereby reducing cellular injury in rat liver.

scholarly journals Oxidative stress-mediated apoptosis of hepatocytes exposed to acute ethanol intoxication

Hepatology ◽  
1997 ◽  
Vol 25 (2) ◽  
pp. 368-378 ◽  
Author(s):  
I Kurose ◽  
H Higuchi ◽  
S Miura ◽  
H Saito ◽  
N Watanabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ethanol Intoxication ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

Role of Hypophysis and Adrenals in Fatty Infiltration of Liver Resulting From Acute Ethanol Intoxication

1955 ◽  
Vol 184 (1) ◽  
pp. 29-34 ◽  
Author(s):  
Samuel Mallov ◽  
Janet L. Bloch
Keyword(s):  
Liver Lipid ◽  
Fatty Infiltration ◽  
Female Rats ◽  
Ethanol Intoxication ◽  
Lipid Response ◽  
Acute Ethanol ◽  
Hypophysectomized Rats ◽  
Acute Ethanol Intoxication ◽  
Prior Administration

Acute ethanol intoxication was found to promote the fatty infiltration of liver in rats. The liver lipid concentrations gradually rose to peak values, then slowly returned to normal. The duration of the fatty infiltration, and the peak liver lipid values obtained, were functions of the dose of ethanol administered. Female rats showed a more severe fatty infiltration than did males, under the same conditions. The prior administration of large quantities of choline reduced the intensity of the fatty infiltration provoked by the ethanol. In contrast to intact animals, neither adrenalectomized nor hypophysectomized rats showed an accumulation of liver lipids as a result of acute ethanol intoxication. Adrenalectomized rats maintained on cortisone, and adrenal demedullated rats, however, showed the same liver lipid response to ethanol as did intact rats. Rats chronically intoxicated for a period of 30 days exhibited hypertrophy of the adrenals. Acute intoxication produced by isopropanol administration also resulted in the accumulation of liver lipid. It is suggested that ethanol intoxication may cause the mobilization of fat from the depots to the liver, and that pituitary and adrenal cortical hormones are involved in the mechanism of this mobilization.

scholarly journals Acute ethanol intoxication induces preferred loss of presynaptic boutons devoid of mitochondria in vivo

2019 ◽  
Author(s):  
Jil Protzmann ◽  
Astha Jaiswal ◽  
Karl Rohr ◽  
Thomas Kuner ◽  
Sidney Cambridge ◽  
...  
Keyword(s):  
Alcohol Intoxication ◽  
Blood Alcohol Concentration ◽  
Memory Loss ◽  
Ethanol Exposure ◽  
Dense Core Vesicle ◽  
Ethanol Intoxication ◽  
Acute Ethanol ◽  
Presynaptic Boutons ◽  
Acute Ethanol Intoxication

AbstractAcute alcohol intoxication is frequently observed in modern societies and carries a vast burden, ranging from traffic accidents to transient memory loss. Despite years of intense research, the effects of acute ethanol intoxication on brain function remain incompletely understood. Here, we studied the effect of acute ethanol intoxication on axonal organelle trafficking and presynaptic structure using in vivo two photon microscopy in anesthetized mice. After a single intraperitoneal injection of ethanol, inducing a blood alcohol concentration of roughly 250 mg/dl, the axonal mitochondrial mobility was doubled while dense core vesicle mobility remained unaffected. Simultaneously imaging mitochondria and presynaptic boutons revealed that unoccupied presynaptic boutons perished more frequently after ethanol exposure, while boutons stably occupied with mitochondria mostly persisted. Our results define a novel mechanism of ethanol action and may explain difficulties in permanently storing new memories after episodes of intense ethanol consumption with a loss of synapses.

scholarly journals The first observation of O2 − generation at real time in vivo from non-Kupffer sinusoidal cells in perfused rat liver during acute ethanol intoxication

FEBS Letters ◽  
1995 ◽  
Vol 372 (2-3) ◽  
pp. 140-143 ◽  
Author(s):  
Minoru Nakano ◽  
Masataka Kikuyama ◽  
Tadashi Hasegawa ◽  
Takashi Ito ◽  
Kazushi Sakurai ◽  
...  
Keyword(s):  
Real Time ◽  
Rat Liver ◽  
Perfused Rat Liver ◽  
Ethanol Intoxication ◽  
Sinusoidal Cells ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

Ethanol-Induced Microaggregate Formation in Pig and Rabbit Blood

1977 ◽  
Vol 37 (02) ◽  
pp. 344-350 ◽  
Author(s):  
Olle Elmér ◽  
Göran Göransson ◽  
Motonori Saku ◽  
Stig Bengmark
Keyword(s):  
Platelet Aggregation ◽  
Direct Effect ◽  
Plasma Proteins ◽  
Chronic Alcoholism ◽  
Ethanol Intoxication ◽  
Pressure Method ◽  
Acute Ethanol ◽  
Acute Ethanol Intoxication

SummaryIncreased microaggregate formation was found after mixing ethanol with blood from pig and rabbit in vitro, measured with Swank’s Screen Filtration pressure method. Final ethanol concentrations were in the range found in ethanol-intoxication in man. No rise in SFP was noticed when plasma with 10,000 platelets/μl was used. It is therefore doubtful that altered plasma proteins caused the rise in SFP. It is suggested that if a direct effect of ethanol upon platelet aggregation exists in vivo, it may be of importance in acute ethanol intoxication and in chronic alcoholism.

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