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Virucidal levels of ozone induce hemolysis and hemoglobin degradation
Author(s) -
Wagner S.J.,
Wagner K.F.,
Friedman L.I.,
Benade L.F.
Publication year - 1991
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1991.31892023502.x
Subject(s) - hemolysis , ozone , hemoglobin , hematocrit , virus , chemistry , incubation , red blood cell , red cell , vesicular stomatitis virus , extracellular , microbiology and biotechnology , biology , virology , immunology , biochemistry , medicine , organic chemistry , endocrinology
The animal virus, vesicular stomatitis virus (VSV), and the bacterial virus, phi 6, were inactivated by greater than 4 log10 in response to incubation with 13 to 14 mL of 1.4 mmol per L (65 micrograms/mL) to 1.6 mmol per L (75 micrograms/mL) of overlaid ozone in virus‐spiked, dilute, red cell suspensions. Virus inactivation was greatly inhibited when ozone was overlaid in the presence of high‐hematocrit red cells or, to a lesser degree, high levels of plasma. At hematocrits at which 5 to 6 log10 of VSV were inactivated, ozone caused 30‐percent hemolysis, as measured by the loss of total cellular hemoglobin. Unexpectedly, this level of hemolysis could not be observed in supernatants because of the ozone‐induced destruction (bleaching) of extracellular hemoglobin. These results suggest that ozone may have little biological specificity for damaging viruses over red cells.