Furthermore, deletion of the hapC gene led to an impaired oxidative stress response.

Activated neutrophils and monocytes from patients displayed impaired oxidative burst.

Both mutations significantly impaired oxidative phosphorylation rates in vivo and membrane ATPase and ATP-driven proton-pumping activities in vitro.

Purpose: Accumulation of mitochondrial DNA deletions and the resultant impaired oxidative phosphorylation may play a pathogenic role in the mediation of age-related sarcopenia.