ArticleToxicology research2023
The potential role of upregulated PARP-1/RIPK1 expressions in amikacin-induced oxidative damage and nephrotoxicity in Wistar rats.
Article in Toxicology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- The synergistic protective effects of bioactive catechins in longjing tea: alleviate indomethacin-induced gastric toxicity through modulation of inflammatory and apoptotic pathways.Frontiers in pharmacology · 2026Article
- NADTrends in molecular medicine · 2025Review
- Daflon and Centrum mitigate vancomycin-induced nephrotoxicity in rats by ameliorating oxidative stress, DNA damage, apoptosis, and inflammation.Frontiers in toxicology · 2025Article
- Tanshinone ⅡA Inhibits Alveolar Macrophage Polarization, Inflammation and Mitochondrial Damage by Regulating the PAPR-1 Signaling Pathway.Iranian journal of pharmaceutical research : IJPRArticle
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
This study aimed to investigate the gene expression levels associated with nephrotoxic action of amikacin, as well as the post-treatment effect of diuretics on its nephrotoxic effects. Sixty male rats were divided equally into six groups, including the control group receiving saline intra-peritoneally (ip), and the five treated groups including therapeutic and double therapeutic dose groups, injected ip (15 and 30 mg/kg b.wt./day) respectively for seven days, and another two rat groups treated as therapeutic and double therapeutic dose groups then administered the diuretic orally for seven days and the last group received amikacin ip at a rate of 15 mg/kg/day for seven days, then given free access to water without diuretics for another seven days and was kept as a self-recovery group. Amikacin caused kidney injury, which was exacerbated by the double therapeutic dose, as evidenced by abnormal serum renal injury biomarkers, elevated renal MDA levels, inhibition of renal catalase and SOD enzyme activities, with renal degenerative and necrotic changes. Moreover, comet assays also revealed renal DNA damage. Interestingly, amikacin administration markedly elevated expression levels of the
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