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Chronic Alcohol Consumption and its Effects on the Cardiac Apoptosis
Author(s) -
Etoundi Clementine,
Haddad George,
Mark Burke
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.975.3
Subject(s) - alcohol , medicine , ventricle , endocardium , apoptosis , endocrinology , cardiology , physiology , pathology , chemistry , biochemistry
Alcohol is a product that has been used by virtually all cultures for rituals, worship, antibacterial and analgesic properties. Clinically, excessive alcohol use increases the risk of liver and heart disease, and other facets of morbidity and mortality. Alternatively, low alcohol has been shown to possess protectant cardiovascular properties while high alcohol has been linked to heart pathology. This experiment focused on potential impact of apoptosis interceding with cardiac effects of chronic high alcohol versus low alcohol exposure. Fraternal rats were pair fed with a liquid diet (Liber‐Dicarli) supplemented with either none, low or high alcohol (5mM or 100mM EtOH) for 5 months. Anesthetized with 5% halothane and excised for retrograde perfusion with PBS, after which hearts were fixed with PFA, and mounted on the cryostat. 30 micron sections of hearts tissue were put in wells with antifreeze, others placed on slides and stained using the cresyl violet procedure. Immunohistochemistry with caspase‐3/7 antibody was performed on free floating sectioned heart tissue from the high and low alcohol heart and control groups to visualize the effects on apoptosis. Chronic high alcohol caused a thinning of left ventricular wall and the enlargement of the ventricle lumen compared to chronic low alcohol and control groups. The caspase‐3/7 immunoreactivity was evident in papillary muscle and endocardium but less evident in the myocardium and epicardial layers. Chronic high alcohol consumption activated adverse cardiac effects initiated by endocardial apoptosis while chronic low alcohol enhanced cellular capacity for survival.