Binge Drinking During Adolescence Induces Long-Lasting Oxidative Stress and Inflammation in the Heart and Promotes Cardiac Dysfunction in Rats.
5 affiliations
- 1Instituto de Ciencias Biomédicas, Facultad de Ciencias de la Salud, Universidad Autónoma de Chile, Santiago 8580000, Chile.
- 2Laboratory of Cardiorespiratory Control, Pontificia Universidad Catolica de Chile, Santiago 8580000, Chile.
- 3Centro de Excelencia en Biomedicina de Magallanes (CEBIMA), Universidad de Magallanes, Punta Arenas 6200000, Chile.
- 4Center for Aging Research and Healthy Longevity, Faculty of Sciences, Universidad Mayor, Santiago 8580745, Chile.
- 5Department of Cell Biology and Physiology, School of Medicine, University of Kansas Medical Center, Kansas City, KS 66160, USA.
Abstract
Background: It is not well-known whether cardiovascular alterations elicited by adolescent binge drinking (ABD) are reversible or if they persist following long-term abstinence until adult life. Thus, we studied the long-term impact of ABD on oxidative stress, inflammation and cardiovascular function. Methods: Twenty-four adolescent Sprague-Dawley rats underwent a controlled or ABD-like protocol, (ethanol 3.00 g/kg i.p.) starting at postnatal day 25 (PND25) to PND38, followed by long-term abstinence until PND70 (adulthood). Results: ABD resulted in overt cardiac dysfunction in adult rats. We found a decreased left ventricular compliance as evidenced by a marked reduction in the early-to-late mitral valve blood flow (E/A: 1.23 ± 0.14 vs. 1.51 ± 0.09, control vs. ABD, p < 0.05). Importantly, cardiac dysfunction was closely linked to adverse cardiac remodeling and fibrosis in ABD animals compared to control animals. Furthermore, we found that ABD resulted in a significant increase in cardiac arrhythmogenesis. Indeed, ABD rats showed a 2-fold increase in the incidence of cardiac arrhythmias compared to control rats (53.6 ± 12.7 vs. 21.7 ± 5.7 events/h, Control vs. ABD, p < 0.05). Finally, we found that cardiac functional impairments were accompanied by increases in cardiac tissue oxidative stress and upregulated levels of pro-inflammatory cytokines (i.e., IL-1β and TNF-α). Conclusions: Present results show that ABD drives long-lasting cardiac dysfunction that persists during early adulthood. Oxidative stress and inflammation may contribute to long-term cardiovascular alterations induced by ABD.
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BibTeX
@article{diaz2026binge,
title = {{Binge Drinking During Adolescence Induces Long-Lasting Oxidative Stress and Inflammation in the Heart and Promotes Cardiac Dysfunction in Rats.}},
author = {Hugo S Díaz and Katherine V Pereyra and Karla G Schwarz and Rodrigo Iturriaga and Rodrigo Del Rio},
journal = {Antioxidants (Basel, Switzerland)},
year = {2026},
month = oct,
doi = {10.3390/antiox15101360},
url = {https://europepmc.org/article/MED/42939934},
note = {CC BY},
}
RIS
TY - JOUR
TI - Binge Drinking During Adolescence Induces Long-Lasting Oxidative Stress and Inflammation in the Heart and Promotes Cardiac Dysfunction in Rats.
AU - Hugo S Díaz
AU - Katherine V Pereyra
AU - Karla G Schwarz
AU - Rodrigo Iturriaga
AU - Rodrigo Del Rio
PY - 2026
DA - 2026/10/21
JO - Antioxidants (Basel, Switzerland)
DO - 10.3390/antiox15101360
UR - https://europepmc.org/article/MED/42939934
AB - Background: It is not well-known whether cardiovascular alterations elicited by adolescent binge drinking (ABD) are reversible or if they persist following long-term abstinence until adult life. Thus, we studied the long-term impact of ABD on oxidative stress, inflammation and cardiovascular function. Methods: Twenty-four adolescent Sprague-Dawley rats underwent a controlled or ABD-like protocol, (ethanol 3.00 g/kg i.p.) starting at postnatal day 25 (PND25) to PND38, followed by long-term abstinence until PND70 (adulthood). Results: ABD resulted in overt cardiac dysfunction in adult rats. We found a decreased left ventricular compliance as evidenced by a marked reduction in the early-to-late mitral valve blood flow (E/A: 1.23 ± 0.14 vs. 1.51 ± 0.09, control vs. ABD, p < 0.05). Importantly, cardiac dysfunction was closely linked to adverse cardiac remodeling and fibrosis in ABD animals compared to control animals. Furthermore, we found that ABD resulted in a significant increase in cardiac arrhythmogenesis. Indeed, ABD rats showed a 2-fold increase in the incidence of cardiac arrhythmias compared to control rats (53.6 ± 12.7 vs. 21.7 ± 5.7 events/h, Control vs. ABD, p < 0.05). Finally, we found that cardiac functional impairments were accompanied by increases in cardiac tissue oxidative stress and upregulated levels of pro-inflammatory cytokines (i.e., IL-1β and TNF-α). Conclusions: Present results show that ABD drives long-lasting cardiac dysfunction that persists during early adulthood. Oxidative stress and inflammation may contribute to long-term cardiovascular alterations induced by ABD.
SN - 2076-3921
ER -