Many heart diseases have been linked to oxidative stress in which an overabundance of unstable molecules called reactive oxygen species negatively react with other molecules in the cell. But what happens to the heart when there’s antioxidative stress—the opposite of oxidative stress?
In a study published in the journal Antioxidants & Redox Signaling, researches report that antioxidative stress could have clinical importance in managing heart failure. The lack of these molecules in mice can trigger the enlargement of the heart and diastolic dysfunction when the heart can’t relax enough after each beat.
They used two groups of mice—one group with low and the other high expression of genes for antioxidants in the heart. The mice with high expression of these genes had hypertrophic cardiomyopathy, abnormally high heart ejection fraction, and diastolic dysfunction at six months of age, the equivalent of a 30 year old person. By 18 months of age—the equivalent to roughly 56 years of age in a human—60% of these mice died. Mice with low expression of antioxidant genes had normal survival rates, but developed irreversible damage to the heart by 15 months of age.
The study’s findings, funded by NHLBI, suggest antioxidative stress can damage the heart over time.