Background:　It　is　widely　accepted　that　the　inevitable　leakage　of　electrons　from　mitochondria　during　respiratory　metabolism　is　managed　intracellularly　through　a　complex　cascade　involving　the　conversion　and　transport　of　reactive　oxygen　species　(ROS)　and　antioxidant　mechanisms.　However,　considering　that　electrons　can　travel　through　various　media,　including　biomacromolecules,　do　leaked　electrons　from　the　electron　transport　chain　necessarily　undergo　complicated　intracellular　disposal　processes?　Here,　we　demonstrate　that　leaked　electrons　may　actually　be　transported　out　of　the　cell.　Methods:　By　expressing　circularly　permuted　yellow　fluorescent　protein　(cpYFP),　a　superoxide　indicator,　at　the　microtubules,　actin,　and　integrin　of　human　embryonic　lung　fibroblasts.　Results:　All　three　corresponding　transgenic　strains　emitted　fluorescent　light,　illuminating　an　ROS　pathway　from　mitochondria　to　the　outer　cell　membrane.　The　fluorescent　intensity　was　positively　correlated　with　mitochondrial　superoxide　content　and　aerobic　respiratory　intensity　but　was　independent　of　cytosolic　ROS　levels.　Conclusion:　These　results　suggest　that　leaked　electrons　are　transported　out　of　the　cell　in　their　electron　form.　We　anticipate　that　our　findings　will　serve　as　a　starting　point　for　revising　the　understanding　of　ROS　generation　and　homeostasis,　implicating　various　physiological　and　pathological　processes.