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Local and systemic increase in lipid peroxidation after moderate experimental traumatic brain injury
Author(s) -
Praticò Domenico,
Reiss Peter,
Tang Lina X.,
Sung Syan,
Rokach Joshua,
McIntosh Tracy K.
Publication year - 2002
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.0022-3042.2002.00777.x
Subject(s) - lipid peroxidation , traumatic brain injury , medicine , urine , urinary system , anesthesia , brain damage , endocrinology , pathology , oxidative stress , psychiatry
Traumatic brain injury is a common event associated with neurological dysfunction. Oxidative damage, may contribute to some of these pathologic changes. We used a specific and sensitive marker of lipid peroxidation, the isoprostane 8,12‐iso‐iPF 2α ‐VI, to investigate whether local and also systemic lipid peroxidation were induced following lateral fluid percussion (FP) brain injury in the rat. Animals were anesthetized and subjected to lateral FP brain injury of moderate severity, or to sham injury as controls. Urine was collected before anesthesia (baseline), 6 and 24 h after injury. Blood was collected at baseline, 1, 6 and 24 h after injury. Animals were killed 24 h after surgery and their brains removed for biochemical analysis. No significant difference was observed at baseline (preinjury) for urine and plasma 8,12‐iso‐iPF 2α ‐VI levels between injured and sham‐operated animals. By contrast, plasma and urinary levels increased significantly already at 1 and further increased 24 h following brain injury, when compared to sham‐operated animals. Finally, compared with sham, injured animals had a significant increase in brain 8,12‐iso‐iPF 2α ‐VI levels. These results demonstrate that moderate brain injury induces widespread brain lipid peroxidation, which is accompanied by a similar increase in urine and plasma. Peripheral measurement of 8,12‐iso‐iPF 2α ‐VI levels after brain injury may be a reliable marker of brain oxidative damage.