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Hemolysis of Human Red Blood Cells by Riboflavin-Cu(II) System: Enhancement by Azide

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Abstract

Photoactivated riboflavin in the presence of Cu(II) generates reactive oxygen species (ROS) which can hemolyze human red blood cells (RBC). In the present work we examined the effect of sodium azide (NaN3) on RBC in the presence of riboflavin and Cu(II). The addition of NaN3 to the riboflavin-Cu(II) system enhanced K+ loss and hemolysis. The extent of K+ loss and hemolysis were time and concentration dependent. Bathocuproine, a Cu(I)-sequestering agent, inhibited the hemolysis completely. Among various free radical scavengers used to identify the major ROS involved in the reaction, thiourea was found to be the most effective scavenger. Thiourea caused almost 85%inhibition of hemolysis suggesting that ·OH is the major ROS involved in the reaction. Using spectral studies and other observations, we propose that when NaN3 is added to the riboflavin-Cu(II) system, it inhibits the photodegradation of riboflavin resulting in increased ·OH generation. Also, the possibility of azide radical formation and its involvement in the reaction could not be ruled out.

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Abbreviations

ROS:

reactive oxygen species

RBC:

red blood cells

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Authors and Affiliations

  1. Faculty of Pharmacy, Applied Science University, Amman, Jordan

    I. Ali & N. Sakhnini

  2. Department of Biochemistry, Faculty of Life Sciences, Aligarh Muslim University, Aligarh, 202002, India

    I. Naseem

Authors
  1. I. Ali
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  2. N. Sakhnini
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  3. I. Naseem
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Correspondence to I. Ali.

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__________

Translated from Biokhimiya, Vol. 70, No. 9, 2005, pp. 1226–1230.

Original Russian Text Copyright © 2005 by Ali, Sakhnini, Naseem.

Originally published in Biochemistry (Moscow) On-Line Papers in Press, as Manuscript BM04-240, December 26, 2004.

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Ali, I., Sakhnini, N. & Naseem, I. Hemolysis of Human Red Blood Cells by Riboflavin-Cu(II) System: Enhancement by Azide. Biochemistry (Moscow) 70, 1011–1014 (2005). https://doi.org/10.1007/s10541-005-0217-x

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  • DOI: https://doi.org/10.1007/s10541-005-0217-x

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