Alteration of the ADP/ATP translocase isoform pattern improves ATP expenditure in developing rat liver mitochondria.

The expression of adenine nucleotide translocase isoforms (AAC) during perinatal development of the rat was studied by measuring mRNA transcript levels of AAC1 and AAC2 genes in liver, heart and brain tissue. In contrast to heart and brain, AAC1 mRNA is not present in adult liver tissue, but is transiently expressed around birth. AAC1 expression in liver did not respond to cold stress (examined with adult rats), therefore a possible involvement of AAC1 in the liver thermogenesis of newborns is excluded. Measurement of the [3H]ADP uptake by liver mitochondria revealed that the molecular activity of the AAC protein was significantly higher in mitochondria from 4-day-old neonates compared with adults. We suggest that the transient AAC1 gene expression in the perinatal liver helps to accommodate the mitochondrial ATP supply to the increased cytosolic ATP consumption initiated at birth.