Thromb Haemost 1997; 77(02): 294-297
DOI: 10.1055/s-0038-1655956
Original Article
Schattauer GmbH Stuttgart

Qualitative Platelet 12-Lipoxygenase Abnormality in a Patient with Essential Thrombocythemia

Authors

  • Kenjiro Tomo

    1   The First Division, Department of Internal Medicine, Tokushima University School of Medicine, Tokushima, Japan
  • Hiroshi Takayama

    1   The First Division, Department of Internal Medicine, Tokushima University School of Medicine, Tokushima, Japan
  • Yoshiyuki Kaneko

    2   Department of Clinical Molecular Biology, Faculty of Medicine, Kyoto University, Kyoto, Japan
  • Jun Fujita

    2   Department of Clinical Molecular Biology, Faculty of Medicine, Kyoto University, Kyoto, Japan
  • Michihiro Nakamura

    3   Department of Biochemistry, Tokushima University School of Medicine, Tokushima, Japan
  • Natsuo Ueda

    3   Department of Biochemistry, Tokushima University School of Medicine, Tokushima, Japan
  • Shozo Yamamoto

    3   Department of Biochemistry, Tokushima University School of Medicine, Tokushima, Japan
  • Minoru Okuma

    1   The First Division, Department of Internal Medicine, Tokushima University School of Medicine, Tokushima, Japan
Further Information

Publication History

Received 21 December 1995

Accepted after revision 08 October 1996

Publication Date:
10 July 2018 (online)

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Summary

Quantitative platelet 12-lipoxygenase (12-LOX) deficiency has been reported in some patients with myeloproliferative disorders (MPD). We report here for the first time a novel qualitative abnormality of the 12-LOX enzyme of platelets from a patient with essential thrombocythemia. The anti-12-LOX immunoprecipitates from the patient’s platelet homogenates showed a deficiency of 12-LOX activity, but contained normal amount of 12-LOX protein. There was no difference in subcellular localization of the enzyme between the patient’s platelets and normal ones. This 12-LOX protein lacking its enzyme activity showed slightly larger electrophoretic mobility than normal one, suggesting a molecular abnormality of the enzyme. However, we could not detect any genetic mutation causing such abnormalities in all exons of 12-LOX gene by sequencing the patient’s PCR-amplified DNA. Thus, our results indicate that the deficient activity of this abnormal 12-LOX protein is probably due to a posttranslational modification, and the possibility that platelets of some MPD patients have qualitative abnormality of the 12-LOX enzyme besides quantitative one.