ABSTRACT
Mitochondrial damage and subsequent loss of adenosine triphosphate are common features of hypoxic and toxic injury in liver. Glycolytic substrates, such as fructose, protect against lethal cell injury from hypoxia in liver. In isolated mitochondria, oxidant chemicals induce a so-called mitochondrial permeability transition. This permeability transition is caused by opening of an unselective pore (minimum diameter 2.8 nm) in the mitochondrial inner membrane of very high conductance, a so-called megachannel. The consequence of the permeability transition is mitochondrial swelling and uncoupling of oxidative phosphorylation. Trifluoperazine protects by blocking the permeability transition and preventing accelerated adenosine triphosphate hydrolysis by uncoupled mitochondria that leads to cell death. Images of the cells were then collected using laser scanning confocal microscopy. The advantage of confocal microscopy over conventional microscopy is that confocal microscopy creates thin optical slices of less than 1 µm in thickness.
