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Mitochondria‐targeted peptide inhibits H2O2‐induced mitochondrial Ca2+ overload in HeLa cells

Treatment of cells with H2O2 leads to Ca2+ release from intracellular stores and result in elevated Ca2+ levels in the cytosol ([Ca2+]c) and mitochondria ([Ca2+]m). Increased [Ca2+]m can result in mitochondria permeability transition (MPT), mitochondrial swelling, cytochrome c release, and apoptosis. A series of aromatic‐cationic peptides developed in this lab were shown to target the inner mitochondrial membrane and prevent calcium‐induced MPT, and inhibit apoptosis in cells treated with t‐butylhydroperoxide. This study was designed to determine if these peptides prevent [Ca2+]m overload in cells treated with H2O2. [Ca2+]m and [Ca2+]c were measured using aequorin targeted to the mitochondria and cytoplasm, respectively. Addition of 1 mM H2O2 caused a rapid rise in both [Ca2+]c and [Ca2+]m. Pretreatment with 1 nM of SS‐19 for 30 minutes prior to addition of 1 mM H2O2 reduced the elevation in [Ca2+]m caused by H2O2 and this was associated with increased [Ca2+]c. These results show that SS‐19 limits mitochondrial calcium loading resulting from H2O2‐induced release of Ca2+ from intracellular stores. Evidence to date suggests that SS‐19 and related peptides prevent Ca2+ overload in mitochondria induced by oxidative stress, maintaining mitochondrial integrity, and protecting against oxidative cell death.