title: Antioxidant mechanisms in apolipoprotein E deficient mice prior to and following closed head injury.
abstract: Apolipoprotein E deficient mice have distinct memory deficits and neurochemical derangements and their recovery from closed head injury is impaired. In the present study, we examined the possibility that the neuronal derangements of apolipoprotein E deficient mice are associated with oxidative stress, which in turn affects their ability to recover from close head injury. It was found that brain phospholipid levels in apolipoprotein E deficient mice 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 higher than those of control mice (132+/-15% of P<0.01). Brains of apolipoprotein E deficient mice had higher Mn-superoxide dismutase (134+/-7%), catalase (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 groups. Closed head injury increased catalase and glutathione peroxidase activities in both mouse groups, whereas glutathione reductase increased only in control mice. The superoxide dismutase activity was unaffected in both groups. These findings suggest that the antioxidative metabolism of apolipoprotein E deficient mice is altered both prior to and following head injury and that antioxidative mechanisms may play a role in mediating the neuronal maintenance and repair derangements of the apolipoprotein E deficient mice.
authors: Department of Neurobiochemistry, George S. Wise Faculty of Life Sciences Tel Aviv University, Tel Aviv, Israel.
authors: L
authors: L
authors: Lomnitski
authors: S
authors: S
authors: Chapman
authors: A
authors: A
authors: Hochman
authors: R
authors: R
authors: Kohen
authors: E
authors: E
authors: Shohami
authors: Y
authors: Y
authors: Chen
authors: V
authors: V
authors: Trembovler
authors: D M
authors: DM
authors: Michaelson
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000032:analysis; D001057:Apolipoproteins E / Q000172:deficiency*; D001205:Ascorbic Acid / Q000032:analysis; D001923:Brain Chemistry; D002374:Catalase / Q000032:analysis; D005978:Glutathione / Q000032:analysis; D005979:Glutathione Peroxidase / Q000032:analysis; D005980:Glutathione Reductase / Q000032:analysis; D005982:Glutathione Transferase / Q000032:analysis; D016489:Head Injuries, Closed / Q000378:metabolism*; D008297:Male; D051379:Mice; D018384:Oxidative Stress; D013482:Superoxide Dismutase / Q000032:analysis
chemical_list: D000975:Antioxidants; D001057:Apolipoproteins E; D002374:Catalase; D005979:Glutathione Peroxidase; D013482:Superoxide Dismutase; D005980:Glutathione Reductase; D005982:Glutathione Transferase; D005978:Glutathione; D001205:Ascorbic Acid