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

Author:

Díaz Alfonso1,Treviño Samuel1,Guevara Jorge2,Muñoz-Arenas Guadalupe1,Brambila Eduardo1,Espinosa Blanca3,Moreno-Rodríguez Albino1,Lopez-Lopez Gustavo1,Peña-Rosas Ulises1,Venegas Berenice4,Handal-Silva Anabella4,Morán-Perales José Luis4,Flores Gonzalo5,Aguilar-Alonso Patricia1

Affiliation:

1. Facultad de Ciencias Químicas, Benemérita Universidad Autónoma de Puebla, 72570 Puebla, PUE, Mexico

2. Departamento de Bioquímica, Facultad de Medicina, Universidad Nacional Autónoma de México, 04510 Ciudad de México, DF, Mexico

3. Departamento de Bioquímica, Instituto Nacional de Enfermedades Respiratorias, 14080 Ciudad de México, DF, Mexico

4. Departamento de Biología y Toxicología de la Reproducción, Instituto de Ciencias, Benemérita Universidad Autónoma de Puebla, 72570 Puebla, PUE, Mexico

5. Laboratorio de Neuropsiquiatría, Instituto de Fisiología, Benemérita Universidad Autónoma de Puebla, 72570 Puebla, PUE, Mexico

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.

Funder

VIEP-BUAP

Publisher

Hindawi Limited

Subject

Cell Biology,Ageing,General Medicine,Biochemistry

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