Amikacin toxicity revisited: pentoxifylline offers protection in high-risk treatment scenarios

Theodor Bilharz Research Institute

Bibliographic Information

Authors: Moustafa N.; El-latif M.B.A.; Farid A.

Journal: AMB Express

Publisher: Springer Science and Business Media Deutschland GmbH

Publication Date: 22 October 2025

Volume / Issue: Volume 15 / Issue 1

Article No.: 153

ISSN: 21910855

DOI: 10.1186/s13568-025-01949-8

Scopus: View on Scopus

Document Type: Article

Access: All Open Access; Gold Open Access; Green Open Access

Authors and Affiliations

Moustafa N., Biotechnology Department, Faculty of Science, Cairo University, Giza, Egypt; El-latif M.B.A., Environmental Research Department, Theodor Bilharz Research Institute, Giza, Egypt; Farid A., Biotechnology Department, Faculty of Science, Cairo University, Giza, Egypt

Abstract

Amikacin (AMK), a potent aminoglycoside antibiotic, is clinically valuable for severe Gram-negative infections but is limited by its nephrotoxic and hepatotoxic effects, primarily mediated through oxidative stress and inflammation. This study investigated the protective role of pentoxifylline (PTX), a methylxanthine derivative with antioxidant and anti-inflammatory properties, against AMK-induced organ damage in male BALB/c mice. Thirty mice were divided into six groups: control, AMK (100 mg/kg/day), PTX monotherapy (50 or 100 mg/kg/day), and AMK combined with PTX (50 or 100 mg/kg/day). After 28 days, biochemical, oxidative stress, inflammatory, and histopathological analyses were conducted. AMK administration significantly elevated renal (BUN and creatinine) and hepatic (ALT, AST and ALP) markers, increased oxidative stress (MDA), and upregulated inflammatory cytokines (IL-17), alongside histopathological damage in kidney and liver tissues. Co-treatment with PTX, particularly at 100 mg/kg, normalized these parameters, restored antioxidant defenses, reduced inflammation, and preserved tissue architecture. PTX demonstrated dose-dependent efficacy, with the higher dose offering complete protection against AMK-induced toxicity. These findings highlighted PTX’s potential as an adjunctive therapy to mitigate AMK-associated nephrotoxicity and hepatotoxicity, suggesting its clinical utility in optimizing aminoglycoside safety without compromising efficacy. © The Author(s) 2025.

Keywords

Amikacin; Inflammation; Kidney; Liver; Oxidative stress; Pentoxifylline; alanine aminotransferase; alkaline phosphatase; aspartate aminotransferase; creatinine; cytokine; glutathione; interleukin 17; malonaldehyde; pentobarbital; superoxide dismutase; urea; uric acid; adult; animal cell; animal experiment; animal model; animal tissue; antioxidant assay; Article; biochemical analysis; blood analysis; body weight fluctuation; centrifugation; circadian rhythm; controlled study; environmental parameters; enzyme linked immunosorbent assay; epithelial cell line; high risk population; histology; histopathology; inflammatory cell; kidney function; lipid peroxidation; liver cell; liver function; liver tissue; liver toxicity; male; morphological adaptation; mouse; nephrotoxicity; nonhuman; organ damage; power analysis; urea nitrogen blood level

Citation Information

Scopus Citations: 3

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