Propolis Prevents the Effects of Chronic Alcohol Intake on Ocular Tissues

2009 ◽  
Vol 42 (3) ◽  
pp. 147-151 ◽  
Author(s):  
Sinan Emre ◽  
Zümrüt Yılmaz ◽  
Feral Öztürk ◽  
M. Hanifi Emre
Keyword(s):  
Alcohol Intake ◽  
Chronic Alcohol ◽  
Ocular Tissues

Decrease in the Number of Muscarinic Receptors in Rat Pancreas after Chronic Alcohol Intake

1989 ◽  
Vol 64 (4) ◽  
pp. 356-359 ◽  
Author(s):  
Juha M. Grönroos ◽  
Timo Kaila ◽  
Heikki J. Aho ◽  
Timo J. Nevalainen
Keyword(s):  
Muscarinic Receptors ◽  
Alcohol Intake ◽  
Chronic Alcohol ◽  
Rat Pancreas

Chronic alcohol intake and carbachol-induced acute pancreatitis in the rat

1994 ◽  
Vol 46 (2) ◽  
pp. 163-167 ◽  
Author(s):  
Juha M. Grönroos ◽  
Jukka Laine ◽  
Timo Kaila ◽  
Timo J. Nevalainen
Keyword(s):  
Acute Pancreatitis ◽  
Alcohol Intake ◽  
Chronic Alcohol

A narrative review of chronic alcohol-induced atrial fibrillation

2021 ◽  
Author(s):  
Rea Mittal ◽  
Lilly Su ◽  
Devyani Ramgobin ◽  
Ashwani Garg ◽  
Rahul Jain ◽  
...  
Keyword(s):  
Atrial Fibrillation ◽  
Alcohol Use ◽  
Alcohol Intake ◽  
Cardiovascular Complications ◽  
Chronic Alcohol ◽  
Higher Alcohol ◽  
Dependent Relationship ◽  
Increased Risk ◽  
Low Levels ◽  
Dose Dependent

Alcohol use disorder (AUD) is highly prevalent and can lead to many cardiovascular complications, including arrhythmias. Chronic alcohol use has a dose-dependent relationship with incidence of atrial fibrillation (AF), where higher alcohol intake (>3 drinks a day) is associated with higher risk of AF. Meanwhile, low levels of chronic alcohol intake (<1 drink a day) is not associated with increased risk of AF. Mechanistically, chronic alcohol intake alters the structural, functional and electrical integrity of the atria, predisposing to AF. Increased screening can help identify AUD patients early on and provide the opportunity to educate on chronic alcohol use related risks, such as AF. The ideal treatment to reduce risk of incident or recurrent AF in AUD populations is abstinence.

β-Sitosterol attenuates liver injury in a rat model of chronic alcohol intake

2020 ◽  
Vol 43 (11) ◽  
pp. 1197-1206
Author(s):  
Zhenjuan Chen ◽  
Ancheng Wu ◽  
Hongmei Jin ◽  
Fuhui Liu
Keyword(s):  
Liver Injury ◽  
Rat Model ◽  
Alcohol Intake ◽  
Chronic Alcohol

Parkin deficiency accentuates chronic alcohol intake-induced tissue injury and autophagy defects in brain, liver and skeletal muscle

2020 ◽  
Vol 52 (6) ◽  
pp. 665-674
Author(s):  
Hu Peng ◽  
Xing Qin ◽  
Sainan Chen ◽  
Asli F Ceylan ◽  
Maolong Dong ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Parkinson’S Disease ◽  
Insulin Sensitivity ◽  
Mitochondrial Respiration ◽  
Alcohol Intake ◽  
Liver Enzymes ◽  
Rectus Femoris ◽  
Protein Carbonyl ◽  
Organ Injury ◽  
Chronic Alcohol

Abstract Alcoholism leads to organ injury including mitochondrial defect and apoptosis with evidence favoring a role for autophagy dysregulation in alcoholic damage. Parkin represents an autosomal recessive inherited gene for Parkinson’s disease and an important member of selective autophagy for mitochondria. The association between Parkinson’s disease and alcoholic injury remains elusive. This study aimed to examine the effect of parkin deficiency on chronic alcohol intake-induced organ injury in brain, liver and skeletal muscle (rectus femoris muscle). Adult parkin-knockout (PRK−/−) and wild-type mice were placed on Liber-De Carli alcohol liquid diet (4%) for 12 weeks prior to assessment of liver enzymes, intraperitoneal glucose tolerance, protein carbonyl content, apoptosis, hematoxylin and eosin morphological staining, and mitochondrial respiration (cytochrome c oxidase, NADH:cytochrome c reductase and succinate:cytochrome c reductase). Autophagy protein markers were monitored by western blot analysis. Our data revealed that chronic alcohol intake imposed liver injury as evidenced by elevated aspartate aminotransferase and alanine transaminase, glucose intolerance, elevated protein carbonyl formation, apoptosis, focal inflammation, necrosis, microvesiculation, autophagy/mitophagy failure and dampened mitochondrial respiration (complex IV, complexes I and III, and complexes II and III) in the brain, liver and rectus femoris skeletal muscle. Although parkin ablation itself did not generate any notable effects on liver enzymes, insulin sensitivity, tissue carbonyl damage, apoptosis, tissue morphology, autophagy or mitochondrial respiration, it accentuated alcohol intake-induced tissue damage, apoptosis, morphological change, autophagy/mitophagy failure and mitochondrial injury without affecting insulin sensitivity. These data suggest that parkin plays an integral role in the preservation against alcohol-induced organ injury, apoptosis and mitochondrial damage.

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