Abstract
Alcoholism causes deleterious effects such as physiological and neuronal alterations leading to the cognitive and other behavioral impairments. Mitochondrial and synaptosomal deteriorations in the brain of alcoholic persons exhibited metabolic, biochemical changes and other related risk factors, which mainly affect the brain function. This study aimed to assess the effect of chronic alcohol-induced mitochondrial and synaptosomal oxidative damage along with behavioral impairment in adult zebrafish. Zebrafish of control group received the system water and normal diet ad libitum (group I); the other groups were treated with 0.20% alcohol (group II) and 0.40% alcohol (group III) directly in fish tank for 22 days. The result revealed significant increase in lipid peroxidation, protein carbonylation, superoxide dismutase, and glutathione, and significant decline in the activity of catalase and Na+/K+ ATPase compared to control. Furthermore, the alcohol-treated zebrafish also showed significant behavioral alterations. Collectively, this regulatory mechanism demonstrates the effect of long-term alcohol consumption in the zebrafish. Our results indicate that this recreational drug “alcohol” is harmful to brain mitochondria and synaptosomes, which are the main organelles, and play an important role in memory, learning, cognitive function, and ATP formation in the brain, which may represent a significant public health concern.
Get full access to this article
View all access options for this article.
References
Supplementary Material
Please find the following supplemental material available below.
For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.
For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.
