L-cysteine protective effects against platelet disaggregation and echinocyte occurrence in gentamicin-induced kidney

Damir Suljević1, Maja Mitrašinović-Brulić2, Muhamed Fočak2

  • 1Department of Biology, Faculty of Science, University of Sarajevo, Zmaja od Bosne 33-35, 71000, Sarajevo, Bosnia and Herzegovina. suljevic.damir@gmail.com.

Insights

Gentamicin antibiotic causes kidney damage and blood cell abnormalities in rats. L-cysteine may help prevent and treat these gentamicin-induced issues.

Area of Science:

  • Toxicology
  • Pharmacology
  • Nephrology

Background:

  • Gentamicin (GM), an aminoglycoside antibiotic, is known to induce nephrotoxicity, leading to acute tubular necrosis and renal failure.
  • GM causes damage to renal proximal tubule cells, resulting in significant morphological and biochemical alterations in blood cells.

Purpose of the Study:

  • To investigate the protective effects of L-cysteine (Cys) against gentamicin-induced nephrotoxicity and associated hematological changes in male Wistar rats.
  • To evaluate the impact of Cys on biochemical parameters and blood cell morphology following GM administration.

Main Methods:

  • Rats were divided into four groups: control, GM-only, Cys-GM, and Cys-GM-Cys.
  • Animals received intraperitoneal injections of saline, GM, or combinations of Cys and GM.
  • Blood samples were analyzed for biochemical and hematological parameters six days post-treatment.

Main Results:

  • Gentamicin administration significantly increased urea and creatinine levels, while decreasing total proteins, albumin, and the albumin/globulin ratio.
  • GM induced lymphocytopenia, thrombocytopenia, neutrophilia, echinocytosis, and platelet disaggregation.
  • GM-induced renal injury correlated with erythrocyte abnormalities, impaired platelet aggregation, and altered plasma biochemical profiles.

Conclusions:

  • Gentamicin-induced nephrotoxicity leads to significant biochemical plasma changes and erythrocyte membrane damage, potentially causing anemia.
  • L-cysteine shows promise as a therapeutic agent for preventing and treating gentamicin-induced renal injury and related blood cell disorders.