Diesel exhaust particle exposure exacerbates contractile dysfunction in diabetic‐like cardiomyocytes

Abstract

Diesel particulate matter (DEP) pollution and diabetes mellitus (DM) are two key contributors to heart disease in modern cities. The purpose of the present study was to evaluate contractile function, calcium signaling and reactive oxygen species (ROS) formation in adult rat ventricular myocytes exposed to DEP (1 μM) and/or DM simulation media (HG, 25.5mM glucose) overnight. Ventricular myocytes were isolated from adult male Sprague‐Dawley rats and sarcomeric contractile properties were evaluated using an IonOptix Field‐Stimulator system, including: peak shortening normalized to baseline (PS), maximal velocities of shortening/relengthening (±dL/dt), time‐to‐90% peak (TPS90,), time‐to‐ 90% relengthening (TR90), change in fura fluorescence intensity (FFI) and fluorescence decay rate (tau). Intracellular ROS formation was assessed using dihydroethidium. We found that DEP exposure significantly decreased PS, ±dL/dt and increased time‐to‐ 90% relengthening (TR90), tau and intracellular ROS formation in diabetic‐like cells. Further studies indicated that antioxidant co‐culture (0.25 mM Tiron and 0.5 mM N‐Acetyl‐L‐cysteine) completely restored contractile function in DEP‐treated diabetic‐like myocytes. Our final data confirm that DEP exacerbates myocardial dysfunction in diabetic cardiomyocytes, which is mediated by ROS production.