Metallothionein prevents diabetes-induced deficits in cardiomyocytes by inhibiting reactive oxygen species production. Diabetes 2003;52(3):777–83

Many individuals with diabetes experience impaired cardiac contractility that cannot be explained by hyper-tension and atherosclerosis. This cardiomyopathy may be due to either organ-based damage, such as fibrosis, or to direct damage to cardiomyocytes. Reactive oxygen species (ROS) have been proposed to contribute to such damage. To address these hypotheses, we examined contractility, Ca2 handling, and ROS levels in individ-ual cardiomyocytes isolated from control hearts, dia-betic OVE26 hearts, and diabetic hearts overexpressing antioxidant protein metallothionein (MT). Our data showed that diabetic myocytes exhibited significantly reduced peak shortening, prolonged duration of short-ening/relengthening, and decreased maximal velocities of shortening/relengthening as well as slowed intracel