Commentary: Sulfur Dioxide Contributes to the Cardiac and Mitochondrial Dysfunction in Rats

A commentary on Sulfur dioxide contributes to the cardiac and mitochondrial dysfunction in rats A commentary on Sulfur dioxide contributes to the cardiac and mitochondrial dysfunction in rats The article by Qin et al. showed that sulfur dioxide contributes in the impairment of cardiac and mitochondrial function in rat H9C2 transformed cardiomyoblasts (1). The authors investigated the effect of 10–100 μM sodium bisulfite (NaHSO3) on the mitochondrial function of H2C9 cells and rat primary cardiomyocytes and showed that COX activities, Δψm, and ATP content were decreased by sulfite (1). This evidence, though restricted to an in vitro cell model, should raise a fundamental concern about sulfite preservatives used in wine industry or food and the consequent role of grapes-derived flavonoids in human health. Actually, one of the main sources of sulfites in the human body comes from the addition of sulfites and sulfur dioxide to many food products. The pejorative effect of sulfite preservatives may dampen the beneficial action of wine polyphenols. Sulfur dioxide dramatically alters grapes transcriptome, leading to mitochondria impairment and downregulation of redox homeostasis (2). Therefore, the presence of sulfur dioxide in plant sources represents an important issue for toxicology, besides any further concern about environmental pollutants. Yet, sulfur dioxide in many conventional, purchasable red wines might not alter necessarily the yield of flavonoids, such as resveratrol, when compared to sulfite-deprived organic wines (3); therefore, its presence or removal should be conventionally reappraised and related to the role than sulfites may have on human health. Yet, toxicology of this food preservative shows many controversial questions in medicine. Although it was considered as an important risk factor for the initiation and progression of liver diseases, based on its proapoptotic and oxidative stressing potential , molecular research on the apoptotic effect of sub-toxicological doses of sulfur dioxide did not appear to fulfill any good expectation, as a controversial debate may occur (4). Figure 1 shows how sulfur dioxide, sulfites, and S-sulfonation of proteins may have different effects on mitochondria and redox signaling. Yet, severe liver injury and necrotic foci were described with the exposure of sulfur dioxide between 56 and 168 mg/m 3 , i.e., within the range 20–60 ppm (5), though far away from the value of 1.5–5.0 ppm, reported by Qin et al. (1). As the same authors addressed in their article, plasma level of sulfites closely depends on dietary habits and the composition of human gut …