Toxic Effects of Intracellular Free Zinc Ion in Cardiomyocytes via Zinc-Transporters: Structural and Functional Changes in Mitochondria

Zinc, a redox inactive element. is accepted as a component of the antioxidant defense system and contributes to maintaining the cell redox balance and endogenous processes, in part, associated with its effect on mitochondria. Mitochondria play vital roles in all alive cells including cardiomyocytes. Under physiological conditions, mitochondria mainly function to provide the required energy to the beating heart by producing ATP and controlling the level of reactive oxygen species (ROS) production. Since several studies demonstrated the relationship between high free Zn2+ levels ([Zn2+]) in cells and increased ROS production, great attention focused on the events related to mechanisms and ways responsible for cellular [Zn2+] homeostasis. Most of the studies also demonstrated the important responsibility of Zn2+-transporters (ZIPs and ZnTs) which control the [Zn2+] homeostasis. Some of these transporters are localized into membranes of not only the sarcoplasmic reticulum but also mitochondria. Their protein expression levels and localizations can change under pathophysiological conditions such as exposure to high ROS in cardiomyocytes. In the present chapter, we aimed to document the toxic effects of intracellular [Zn2+] in cardiomyocytes via the contribution of altered levels of Zn2+-transporters, particularly associated with those of localize into mitochondria and induce changes in the structure and function of mitochondria.