Closed Head Injury in the Rat Induces Whole Body Oxidative Stress: Overall Reducing Antioxidant Profile

Traumatic injury to the brain triggers the accumulation of harmful mediators, including highly toxic reactive oxygen species (ROS). Endogenous defense mechanism against ROS is provided by low molecular weight antioxidants (LMWA), reflected in the reducing power of the tissue, which can be measured by cyclic voltammetry (CV). CV records biological peak potential (type of scavenger), and anodic current intensity (scavenger concentration). The effect of closed head injury (CHI) on the reducing power of various organs was studied. Water and lipid soluble extracts were prepared from the brain, heart, lung, kidney, intestine, skin, and liver of control and traumatized rats (1 and 24 h after injury) and total LMWA was determined. Ascorbic acid, uric acid, alpha-tocopherol, carotene and ubiquinol-10 were also identified by HPLC. The dynamic changes in LMWA levels indicate that the whole body responds to CHI. For example, transient reduction in LMWA (p0.01) in the heart, kidney, lung and liver at 1 h suggests their consumption, probably due to interaction with locally produced ROS. However, in some tissues (e.g., skin) there was an increase (p0.01), arguing for recruitment of higher than normal levels of LMWA to neutralize the ROS. alpha-Tocopherol levels in the brain, liver, lung, skin, and kidney were significantly reduced (p0.01) even up to 24 h. We conclude that although the injury was delivered over the left cerebral hemisphere, the whole body appeared to be under oxidative stress, within 24 h after brain injury.