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Research Article| Volume 89, ISSUE 3, P581-591, March 1977

Decreased surface charge and accelerated senescence of red blood cells following neuraminidase treatment

  • Stephen A. Landaw
    Correspondence
    Reprint requests: Stephen A. Landaw, M.D., Ph.D., Associate Chief of Staff, Research, V.A. Hospital, Irving Ave. and University Place, Syracuse, N. Y. 13210.
    Affiliations
    From the Donner Laboratory, University of California, Berkeley, Calif. U.S.A.

    From the V.A. Hospital, Syracuse, N. Y. U.S.A.
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  • Tom Tenforde
    Affiliations
    From the Donner Laboratory, University of California, Berkeley, Calif. U.S.A.

    From the V.A. Hospital, Syracuse, N. Y. U.S.A.
    Search for articles by this author
  • John C. Schooley
    Affiliations
    From the Donner Laboratory, University of California, Berkeley, Calif. U.S.A.

    From the V.A. Hospital, Syracuse, N. Y. U.S.A.
    Search for articles by this author
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      Abstract

      Female LAF1 mice were given single or repeated injections of V. cholerae N'ase and the effects on circulating RBC surface charge and life span were determined. Intravenous injection of N'ase caused a rapid decrease in RBC surface charge of approximately 14 percent, and survival of such treated cells was reduced by approximately one fifth by virtue of an acceleration of senescence. When RBC's were treated in vitro with N'ase, a comparable (14 to 17 percent) reduction in surface charge was seen. Such cells, when injected into intact mice, showed a similar acceleration of senescence. When N'ase was injected intravenously into splenectomized mice, RBC survival was similar to that of controls. Intravenous injection of N'ase 1 hour before injection of labeled RBC's did not alter RBC survival nor did it accelerate the clearance of carbon particles by the RES. These results indicate that N'ase accelerates senescence in treated mouse erythrocytes by acting on the RBC's and not by activating the RES. Absence of this effect in splenectomized mice implicates the spleen as the sensor of the induced alterations in surface charge. These results and those recently reported for treated RBC's in the dog, rat, rabbit, and man suggest that at least a portion of the phenomenon of RBC senescence may be related to the loss of RBC surface charge.
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