Levofloxacin induces erythrocyte contraction leading to red cell death

Authors

  • Hafiz Muhammad Aslam Department of Biochemistry, University of Agriculture Faisalabad - Pakistan image/svg+xml https://orcid.org/0009-0002-5252-1214
  • Azka Sohail Department of Biochemistry, University of Agriculture Faisalabad - Pakistan image/svg+xml
  • Ammara Shahid Department of Internal Medicine, Amna Anayat Medical College, Sheikhupura - Pakistan
  • Maham Abdul Bari Khan Department of Biochemistry, University of Agriculture Faisalabad - Pakistan image/svg+xml https://orcid.org/0009-0004-6520-5215
  • Muhammad Umar Sharif Department of Anatomy, Faculty of Veterinary Science, University of Agriculture Faisalabad - Pakistan image/svg+xml
  • Razia Kausar Department of Anatomy, Faculty of Veterinary Science, University of Agriculture Faisalabad - Pakistan image/svg+xml
  • Samia Nawab Department of Chemistry, Government Graduate College For Women, Township - Lahore
  • Waqas Farooq Institute of Biomedical Sciences, Shanxi University, Taiyuan - China image/svg+xml
  • Kashif Jilani Department of Biochemistry, University of Agriculture Faisalabad - Pakistan image/svg+xml
  • Majeeda Rasheed Department of Life Sciences, Khwaja Fareed University of Engineering and Information Technology Rahimyar Khan, Punjab - Pakistan https://orcid.org/0000-0003-1400-9906

DOI:

https://doi.org/10.33393/dti.2024.3060

Keywords:

Eryptosis, Erythrocyte, Hemolysis, Levofloxacin, Oxidative stress

Abstract

Background: Levofloxacin, a fluoroquinolone, is an extensively used antibiotic effective against both positively and negatively staining bacteria. It works by inhibiting bacterial topoisomerase type II and topoisomerase type IV, resulting in impaired DNA synthesis and bacterial cell death. Eryptosis is another term for apoptotic cell death of erythrocyte marked by cell shrinkage, phosphatidylserine (PS) flipping, and membrane blebbing.

Methods: The intent of the present research was to look at the eryptotic effect of levofloxacin by exposing erythrocytes to therapeutical doses (7, 14 µM) of levofloxacin for 48 hours. Cell size evaluation, PS subjection to outside, and calcium channel inhibition were carried out to investigate eryptosis. Oxidative stress generated by levofloxacin was measured as a putative mechanism of eryptosis using glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase activities. Similarly, hemolysis measurements demonstrated levofloxacin’s cytotoxic effect.

Results: Our findings showed that therapeutic doses of levofloxacin can cause a considerable decline in antioxidant enzymes activities, as well as induce cell shrinkage, PS externalization, and hemolysis in erythrocytes. The role of calcium in triggering erythrocyte shrinkage was also confirmed.

Conclusion: In conclusion, our findings showed that the indicated levofloxacin doses caused oxidative stress, which leads to erythrocyte death via eryptosis and hemolysis. These findings emphasize the importance of using levofloxacin with caution and the need for additional research to mitigate these side effects.

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Published

2024-10-07

How to Cite

Aslam, H. M., Sohail, A., Shahid, A., Khan, M. A. B., Muhammad Umar Sharif, Kausar, R., Nawab, S., Farooq, W., Jilani, D. K., & Rasheed, M. (2024). Levofloxacin induces erythrocyte contraction leading to red cell death. Drug Target Insights, 18(1), 78–83. https://doi.org/10.33393/dti.2024.3060

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Section

Original Research Article

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Received 2024-03-02
Accepted 2024-07-11
Published 2024-10-07

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