Closed head injury in the rat induces whole body oxidative stress: Overallreducing antioxidant profile

Traumatic injury to the brain triggers the accumulation of harmful mediator s, including highly toxic reactive oxygen species (ROS). Endogenous defense mechanism against ROS is provided by low molecular weight antioxidants (LM WA), reflected in the reducing power of the tissue, which can be measured b y cyclic voltammetry (CV). CV records biological peak potential (type of sc avenger), and anodic current intensity (scavenger concentration). The effec t of closed head injury (CHI) on the reducing power of various organs was s tudied. Water and lipid soluble extracts were prepared from the brain, hear t, lung, kidney, intestine, skin, and liver of control and traumatized rats (1 and 24 h after injury) and total LMWA was determined. Ascorbic acid, ur ic acid, a-tocopherol, carotene and ubiquinol-10 were also identified by HP LC. The dynamic changes in LMWA levels indicate that the whole body respond s to CHI. For example, transient reduction in LMWA (p < 0.01) 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 (p < 0.01), 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 (p < 0.01) even up to 24 h. We conclude that although the injury was delivered over t he left cerebral hemisphere, the whole body appeared to be under oxidative stress, within 24 h after brain injury.