White Wine Intake Reduces Mitochondrial Complex I-Derived ROS in the Male Rat Heart

Epidemiological studies suggest that, despite the adverse effects of excessive alcohol intake, low-to-moderate levels of wine consumption have been associated with favorable cardiovascular outcomes. While the biological effects of polyphenol-rich red wine have been extensively studied, less is known about the impact of white wine on myocardial cellular function and the underlying mechanisms. In this study, young male Sprague-Dawley rats were given ad libitum access to white wine or water for four weeks, after which cardiac mitochondrial function, cardiomyocyte susceptibility to oxidative stress, and cardiac transcriptomic profiles were assessed using respirometry, ROS measurements, in vitro oxidative stress assay, and RNA sequencing. White wine consumption did not significantly alter mitochondrial respiratory capacity, expression of antioxidant enzymes or cardiomyocyte survival following oxidative challenge. However, mitochondrial ROS production at respiratory complex I was significantly reduced, particularly during reverse electron transport mimicking ischemia/reperfusion. Transcriptomic analysis revealed modest changes, with no genes meeting the false discovery rate threshold. Analyses based on nominal significance revealed changes associated with mitochondrial electron transfer, protein quality control, apoptosis, and inflammatory signaling. In conclusion, four-week white wine consumption was associated with reduced mitochondrial ROS without impairing cardiac bioenergetics, accompanied by subtle transcriptional responses.