4.5 Article

Local and systemic increase in lipid peroxidation after moderate experimental traumatic brain injury

期刊

JOURNAL OF NEUROCHEMISTRY
卷 80, 期 5, 页码 894-898

出版社

WILEY
DOI: 10.1046/j.0022-3042.2002.00777.x

关键词

isoprostanes; lipid peroxidation; oxidative stress; traumatic brain injury

资金

  1. NATIONAL INSTITUTE OF GENERAL MEDICAL SCIENCES [R01GM034690] Funding Source: NIH RePORTER
  2. NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [P01NS008803, P50NS008803] Funding Source: NIH RePORTER
  3. NIGMS NIH HHS [GM34690] Funding Source: Medline
  4. NINDS NIH HHS [NS08803] Funding Source: Medline

向作者/读者索取更多资源

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(2alpha)-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-FF2alpha-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(2alpha)-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(2alpha)-VI levels after brain injury may be a reliable marker of brain oxidative damage.

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