homeostasis/metabolism
N |
• in response to kidney ischemia-reperfusion injury, mice exhibit a similar infiltration of neutrophils and other leukocytes into kidney tissue (as shown by flow cytometry and myeloperoxidase immunohistochemistry) with comparable LTB4 levels and no significant differences in the degree or extent of renal injury (as assessed by histological scoring and blood urea nitrogen levels) relative to wild-type controls
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• bone marrow neutrophils fail to convert leukotriene B4 (LTB4) to 19-hydroxy LTB4 and to a lesser extent 18-hydroxy LTB4 indicating loss of all LTB4 omega oxidation products, unlike in wild-type neutrophils
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• terminally hydroxylated products of LTB4 metabolism (19-, and 18-hydroxy LTB4) are undetectable in bone marrow neutrophils, unlike in wild-type neutrophils
• however, production of 12-oxo LTB4 (a product of an independent pathway involving 12-hydroxydehydrogenase) is similar to that in wild-type neutrophils
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cellular
• bone marrow neutrophils fail to convert leukotriene B4 (LTB4) to 19-hydroxy LTB4 and to a lesser extent 18-hydroxy LTB4 indicating loss of all LTB4 omega oxidation products, unlike in wild-type neutrophils
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