Redox regulation of calcium signaling in cancer cells by ascorbic Acid involving the mitochondrial electron transport chain.

Previously, we have reported that ascorbic acid regulates calcium signaling in human larynx carcinoma HEp-2 cells. To evaluate the precise mechanism of Ca(2+) release by ascorbic acid, the effects of specific inhibitors of the electron transport chain components on mitochondrial reactive oxygen species (ROS) production and Ca(2+) mobilization in HEp-2 cells were investigated. It was revealed that the mitochondrial complex III inhibitor (antimycin A) amplifies ascorbate-induced Ca(2+) release from intracellular stores.

Redox buffer capacity of the cell: theoretical and experimental approach.

Reactive oxygen species (ROS) are involved in a variety of biological phenomena, such as mutation, carcinogenesis, inflammation, aging, development, and signal transduction. Intracellular generation of ROS might lead to the activation of redox signaling or oxidative stress. Nonetheless, it is difficult to estimate whether ROS-induced intracellular events are beneficial or deleterious to the cell.