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Leukotriene B 4 Release and Polymorphonuclear Cell Infiltration in Spinal Cord Injury
Author(s) -
Xu Jian,
Hsu Chung Y.,
Liu Tsung H.,
Hogan Edward L.,
Perot Phanor L.,
Tai HsinHsiung
Publication year - 1990
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 - 10.1111/j.1471-4159.1990.tb04577.x
Subject(s) - spinal cord , arachidonic acid , leukotriene , leukotriene c4 , infiltration (hvac) , chemistry , leukotriene b4 , spinal cord injury , myeloperoxidase , cord , arachidonate 5 lipoxygenase , endocrinology , medicine , biochemistry , inflammation , enzyme , surgery , physics , psychiatry , asthma , thermodynamics
Activation of arachidonic acid occurs after spinal cord injury. Leukotriene B 4 is a lipoxygenase metabolite of arachidonic acid. In a rat model of experimental spinal cord injury, we found that the leukotriene B 4 content was less than the sensitivity of our assay (8 pg/mg of protein) in non‐traumatized spinal cord. Leukotriene B 4 was detectable in raumatized cord (mean ± SE, 25 ± 5 pg/mg of protein; n = 3). Release of leukotriene B 4 from spinal cord slices into the incubation medium was also noted after trauma (9 ± 1 pg/mg of protein; n = 12) and was enhanced by exposure of traumatized spinal cord slices to the calcium ionophore A23187 (375 ± 43 pg/mg of protein; n = 12). The amount of leukotriene B 4 released corresponded to the extent of post‐traumatic polymorphonuclear cell infiltration determined by a myeloperoxidase assay. Results from this study suggest that the source of leukotriene B 4 in spinal cord injury is infiltrating polymorphonuclear cells.