The impact of alpha-lipoic acid on amikacin-induced nephrotoxicity

Aşçı, Halil; Saygın, Mustafa; Çankara, Fatma Nihan; Bayram, Dilek; Yeşilot, Şükriye; Candan, İbrahim Aydın; İlhan, İlter

doi:10.3109/0886022x.2014.967645

Cited by 14 publications

(7 citation statements)

References 34 publications

(45 reference statements)

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“…12,13,26 DNA, in particular, is more susceptible to attack by reactive oxygen species than proteins and membrane lipids, which are protected by lowmolecular weight anti-oxidants and anti-oxidant enzymes. Among many types of oxidative DNA damage, 8-OHdG is one of the most abundant oxidative products of cellular DNA.…”

Section: Discussionmentioning

confidence: 99%

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Bulut

Başbuğan

Arı³

et al. 2016

Renal Failure

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This study aimed to investigate the possible protective effect of paricalcitol on experimental amikacin-induced nephrotoxicity model in rats. Wistar albino rats (n ¼ 32) were allocated into four equal groups of eight each, the control (Group C), paricalcitol (Group P), amikacin-induced nephrotoxicity (Group A), and paricalcitol-treated amikacin-induced nephrotoxicity (Group A þ P) groups. Paricalcitol was given intra-peritoneally at a dose of 0.4 lg/kg/d for 5 consecutive days prior to induction of amikacin-induced nephrotoxicity. Intra-peritoneal amikacin (1.2 g/kg) was used to induce nephrotoxicity at day 4. Renal function parameters, oxidative stress biomarkers, oxidative DNA damage (8-hydroxy-2 0 -deoxyguanosine/deoxyguanosine ratio), kidney histology, and vascular endothelial growth factor (VEGF) immunoexpression were determined. Group A þ P had lower mean fractional sodium excretion (p < 0.001) as well as higher creatinine clearance (p ¼ 0.026) than the amikacin group (Group A). Renal tissue malondialdehyde levels (p ¼ 0.035) and serum 8-hydroxy-2 0 -deoxyguanosine/deoxyguanosine ratio (8-OHdG/dG ratio) (p < 0.001) were significantly lower; superoxide dismutase (p ¼ 0.024) and glutathione peroxidase (p ¼ 0.007) activities of renal tissue were significantly higher in group A þ P than in group A. The mean scores of tubular necrosis (p ¼ 0.024), proteinaceous casts (p ¼ 0.038), medullary congestion (p ¼ 0.035), and VEGF immunoexpression (p ¼ 0.018) were also lower in group A þ P when compared with group A. This study demonstrates the protective effect of paricalcitol in the prevention of amikacin-induced nephrotoxicity in an experimental model. Furthermore, it is the first study to demonstrate that paricalcitol improves oxidative DNA damage in an experimental acute kidney injury model. ARTICLE HISTORY

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Section: Discussionmentioning

confidence: 99%

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Bulut

Başbuğan

Arı³

et al. 2016

Renal Failure

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“…Histopathological studies have shown that tubular necrosis is the main cause of nephrotoxicity (Asci et al 2015;Parlakpinar et al 2004). Glomerulus obstruction, proin ammatory cell migration, tubule dilatation, bleeding, and tubule degeneration were observed in the AK-induced nephrotoxicity group (Asci et al 2015).…”

Section: Discussionmentioning

confidence: 99%

Carvacrol attenuates amikacin-induced nephrotoxicity in the rat

Dost

Gunata

Özhan

et al. 2021

Preprint

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Amikacin (AK) is frequently used in the treatment of gram-negative and some gram-positive infections. However, its use is limited due to nephrotoxicity due to the increase in reactive oxygen radicals. The aim of this study was to investigate the role of carvacrol (CAR) against AK-induced nephrotoxicity in rats. Thirty-two Sprague Dawley rats were randomly divided into four groups as control (Vehicle), AK (400 mg/kg), CAR + AK (80 mg/kg CAR + 400 mg/kg AK), and AK + CAR (400 mg/kg AK + 80 mg/kg CAR) groups. AK and CAR were administered via intramuscular and per-oral for 7 days, respectively. Blood and kidney tissue samples were taken at the end of the experiment. Renal function and histopathological changes were compared, and the relevant parameters of oxidative stress and inflammation were detected. Histopathological findings (necrotic changes and dilatation and inflammatory cell infiltration) significantly increased in the AK group compared to the control group. Also, the rats in the AK group lost weight significantly. It was found that CAR treatment before and after AK significantly improved nephrotoxicity histopathologically (p < 0.05). However, this improvement was not detected biochemically. These results show that CAR treatment before and after AK improves nephrotoxicity in the histopathological level.

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“…As an example of antioxidant drugs, alpha-lipoic acid neutralizes ROS and restores inactivated natural antioxidants, such as vitamin C, with promising results in animal studies [99,100]. Selenium supplementation is proposed to reduce cellular oxidative damage in animal models.…”

Section: Perspectives On Pharmacological Treatmentmentioning

confidence: 99%

Acute kidney injury in pediatrics: an overview focusing on pathophysiology

et al. 2021

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Acute kidney injury (AKI) is defined as an abrupt decline in glomerular filtration rate, with increased serum creatinine and nitrogenous waste products due to several possible etiologies. Incidence in the pediatric population is estimated to be 3.9 per 1,000 hospitalizations, and prevalence among children admitted to intensive care units is 26.9%. Despite being a condition with important incidence and morbimortality, further evidence on pathophysiology and management among the pediatric population is still lacking. This narrative review aimed to summarize and discuss current data on AKI pathophysiology in the pediatric population, considering all the physiological particularities of this age range and common etiologies. Additionally, we reported current diagnostic tools, novel biomarkers, and newly proposed medications that have been studied with the aim of early diagnosis and appropriate treatment of AKI in the future.

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The impact of alpha-lipoic acid on amikacin-induced nephrotoxicity

Cited by 14 publications

References 34 publications

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Paricalcitol may improve oxidative DNA damage on experimental amikacin-induced nephrotoxicity model

Carvacrol attenuates amikacin-induced nephrotoxicity in the rat

Acute kidney injury in pediatrics: an overview focusing on pathophysiology

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