Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury

Apolipoprotein E deficient mice have distinct memory deficits and neurochem ical derangements and their recovery from closed head injury is impaired. I n the present study, we examined the possibility that the neuronal derangem ents of apolipoprotein E deficient mice are associated with oxidative stres s, which in turn affects their ability to recover from close head injury. I t was found that brain phospholipid levels in apolipoprotein E deficient mi ce are lower than those of the controls (55 +/- 15% of control, P < 0.01), that the cholesterol levels of the two mice groups are similar and that the levels of conjugated dienes of the apolipoprotein E deficient mice are hig her than those of control mice (132 +/- 15% of P < 0.01). Brains of apolipo protein E deficient mice had higher Mn-superoxide dismutase (134 +/- 7%), c atalase (122 +/- 8%) and glutathione reductase (167 +/- 7%) activities than control (P < 0.01), whereas glutathione peroxidase activity and the levels of reduced glutathione and ascorbic acid were similar in the two mouse gro ups, Closed head injury increased catalase and glutathione peroxidase activ ities in both mouse groups, whereas glutathione reductase increased only in control mice. The superoxide dismutase activity was unaffected in both gro ups. These findings suggest that the antioxidative metabolism of apolipopro tein E deficient mice is altered both prior to and following head injury an d that antioxidative mechanisms may play a role in mediating the neuronal m aintenance and repair derangements of the apolipoprotein E deficient mice. (C) 1999 Elsevier Science B.V. All rights reserved.