Apoptosis is a process present in a variety of cardiovascular diseases, and oxidative stress is a major apoptotic stimulus in these diseases. Glutathione S-transferase (GST) plays a crucial role against oxidative injury; it also regulates glutathione homeostasis. Recently, new roles for GST have been discussed such as in gene expression, protein glutathionylation and nitric oxide metabolism. However, its role with regard to cardiomyocyte apoptosis and alteration of signalling cascades of cardiomyocytes has not been determined. This article evaluates the effect of GST inhibition on cardiomyocyte apoptosis and on the alteration of proteins and mitogen-activated protein kinase pathways in rat models.