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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.
Abstract:
Gentamicin (GM) is an aminoglycoside antibiotic that induces nephrotoxicity. GM also causes necrosis of cells in the renal proximal tubules, resulting in acute tubular necrosis, followed by acute renal failure. Morphological alteration of blood cells, leukocytes and platelets count, as well as biochemical effects of L-cysteine (Cys) and antibiotic gentamicin, in clinically healthy male Wistar rats, were studied. Rats were divided into four groups: control (injected with 0.9% saline i.p.), GM (80 mg/kg b.w.; gentamicin injected i.p.), Cys-GM (100 mg/kg b.w.; L-cysteine and 80 mg/kg b.w. gentamicin injected i.p.), and Cys-GM-Cys (administered double dosage of 100 mg/kg b.w. L-cysteine and 80 mg/kg b.w. gentamicin i.p.). Biochemical and hematological analyses were performed on blood samples taken six days after treatments. Total proteins, albumin concentration and A/G ratio were significantly lower in experimental groups. Cholesterol, triglycerides, urea, and creatinine concentrations were significantly higher in relation to control. GM-induced lymphocytopenia, thrombocytopenia and neutrophilia. Echinocytosis and platelet disaggregation were found in all GM-treated animals. GM caused renal injury which indirectly led to erythrocyte abnormalities, changes in platelet aggregation, decreased protein fractions, and increased lipid and nitrogen components. The results suggest that GM-induced renal injury leads to significant biochemical changes in blood plasma, erythrocyte membrane impairment which can consequently cause anemia. Therefore, Cys might represent a novel therapeutic tool in the prevention and treatment of gentamicin-induced renal injury and blood cell disorders.
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.

