Cytosolic and mitochondrial Ca concentrations in primary hepatocytes change with ageing and in consequence of an mtDNA mutation.

Mitochondrial Ca flux is crucial for the regulation of cell metabolism. Ca entry to the mitochondrial matrix is mediated by VDAC1 and MCU with its regulatory molecules. We investigated hepatocytes isolated from conplastic C57BL/6NTac-mt mice (mtNOD) that differ from C57BL/6NTac mice (controls) by a point mutation in mitochondrial-encoded subunit 3 of cytochrome c oxidase, resulting in functional and morphological mitochondrial adaptations.

Mitochondrial complex IV mutation increases reactive oxygen species production and reduces lifespan in aged mice.

Aim: Mitochondrial DNA (mtDNA) mutations can negatively influence lifespan and organ function. More than 250 pathogenic mtDNA mutations are known, often involving neurological symptoms. Major neurodegenerative diseases share key etiopathogenetic components ie mtDNA mutations, mitochondrial dysfunction and oxidative stress.