2015 Volume 26 Issue 2 Pages 77-81
The central nervous system (CNS) white matter (WM) ischemia is an important clinical problem and may produce injury, in part, by reactive oxygen species (ROS)-induced mitochondrial dysfunction. Using the mouse optic nerve (MON) WM model, we tested whether hydrogen (H2) in drinking water reduced functional WM ischemic injury. Functional integrity of MON was determined by quantitatively monitoring the area of MON compound action potential (CAP) in vitro. A 60 min period of oxygen and glucose deprivation (OGD) caused prompt loss of the CAP followed by an average 20% recovery. After 10–14 days of H2-water, the CAP area did not disappear during ischemia and recovered to a significantly great extent during reperfusion. Immunostaining of axonal neurofilament also showed significant protection by previous drinking of H2-water. Accumulation of nuclear 8-oxoguanine (8-oxoG), a marker of oxidative DNA damage, was observed mainly in oligodendrocytes after OGD. The level of 8-oxoG and lipid peroxidation after OGD were significantly reduced in optic nerves from H2-water drinking mice. The importance of these observations is that ischemic protection of myelinated CNS WM by drinking H2-water provided partial protection in a novel manner, suggesting oxidative stress-resistance and intriguing therapeutic options.
