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Oxidative Medicine and Cellular Longevity
Volume 2016, Article ID 8725354, 9 pages
http://dx.doi.org/10.1155/2016/8725354
Research Article

Energy Drink Administration in Combination with Alcohol Causes an Inflammatory Response and Oxidative Stress in the Hippocampus and Temporal Cortex of Rats

1Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 72570 Puebla, PUE, Mexico
2Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, 04510 Ciudad de México, DF, Mexico
3Departamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias, 14080 Ciudad de México, DF, Mexico
4Departamento de Biología y Toxicología de la Reproducción, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, 72570 Puebla, PUE, Mexico
5Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, 72570 Puebla, PUE, Mexico

Received 13 October 2015; Revised 21 January 2016; Accepted 8 February 2016

Academic Editor: Javier Egea

Copyright © 2016 Alfonso Díaz et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Energy drinks (EDs) are often consumed in combination with alcohol because they reduce the depressant effects of alcohol. However, different researches suggest that chronic use of these psychoactive substances in combination with alcohol can trigger an oxidative and inflammatory response. These processes are regulated by both a reactive astrogliosis and an increase of proinflammatory cytokines such as IL-1β, TNF-α, and iNOS, causing cell death (apoptosis) at the central and peripheral nervous systems. Currently, mechanisms of toxicity caused by mixing alcohol and ED in the brain are not well known. In this study, we evaluated the effect of chronic alcohol consumption in combination with ED on inflammatory response and oxidative stress in the temporal cortex (TCx) and hippocampus (Hp) of adult rats (90 days old). Our results demonstrated that consuming a mixture of alcohol and ED for 60 days induced an increase in reactive gliosis, IL-1β, TNF-α, iNOS, reactive oxygen species, lipid peroxidation, and nitric oxide, in the TCx and Hp. We also found immunoreactivity to caspase-3 and a decrease of synaptophysin in the same brain regions. The results suggested that chronic consumption of alcohol in combination with ED causes an inflammatory response and oxidative stress, which induced cell death via apoptosis in the TCx and Hp of the adult rats.