Evaluation of efficacy of natural astaxanthin and vitamin E in prevention of colistin-induced nephrotoxicity in the rat model

Ghlissi, Zohra; Hakim, Ahmed; Sila, Assaâd; Mnif, Héla; Zeghal, Khaled Mounir; Rebaï, Tarek; Bougatef, Ali; Sahnoun, Zouheir

doi:10.1016/j.etap.2014.03.004

Cited by 58 publications

(38 citation statements)

References 33 publications

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“…Lycopene has been shown to interact with ROS and thereby to prevent ROSinduced tissue and cellular damage (35). Consistent with previous studies, we revealed that colistin-induced nephrotoxicity is associated with significantly increased MDA levels and a concomitant decrease in the levels of antioxidant enzymes CAT, SOD, and GSH (Table 2) (16,18,60,61). In the present study, lycopene treatment restored the levels of all of these biomarkers to the normal range observed in the untreated control group (Table 2), confirming its nephroprotective effect.…”

Section: Discussionsupporting

confidence: 80%

“…*, P Ͻ 0.05; **, P Ͻ 0.01 (compared to the control group); #, P Ͻ 0.05; ##, P Ͻ 0.01 (compared to the colistin group). [16][17][18]55). Increased production of ROS is an important mechanism in colistin-induced nephrotoxicity and neurotoxicity (17,(56)(57)(58).…”

Section: Discussionmentioning

confidence: 99%

“…Reactive oxygen species (ROS) molecules are mainly generated by mitochondria and are among the major mediators of oxidative stress; they initiate renal cell apoptosis, which finally leads to renal dysfunction (14,15). ROSmediated oxidative stress plays a key role in colistin-induced nephrotoxicity (12,(16)(17)(18).…”

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confidence: 99%

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Lycopene Attenuates Colistin-Induced Nephrotoxicity in Mice via Activation of the Nrf2/HO-1 Pathway

Dai

Tang

Deng

et al. 2015

Antimicrob Agents Chemother

107

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bNephrotoxicity is the major dose-limiting factor for the clinical use of colistin against multidrug-resistant (MDR) Gram-negative bacteria. This study aimed to investigate the protective effect of lycopene on colistin-induced nephrotoxicity in a mouse model. Fifty mice were randomly divided into 5 groups: the control group (saline solution), the lycopene group (20 mg/kg of body weight/day administered orally), the colistin group (15 mg/kg/day administered intravenously), the colistin (15 mg/kg/day) plus lycopene (5 mg/kg/day) group, and the colistin (15 mg/kg/day) plus lycopene (20 mg/kg/day) group; all mice were treated for 7 days. At 12 h after the last dose, blood was collected for measurements of blood urea nitrogen (BUN) and serum creatinine levels. The kidney tissue samples were obtained for examination of biomarkers of oxidative stress and apoptosis, histopathological assessment, and quantitative reverse transcription-PCR (qRT-PCR) analysis. Colistin treatment significantly increased concentrations of BUN and serum creatinine, tubular apoptosis/necrosis, lipid peroxidation, and heme oxygenase 1 (HO-1) activity, while the treatment decreased the levels of endogenous antioxidant biomarkers glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD). Notably, the changes in the levels of all biomarkers were attenuated in the kidneys of mice treated with colistin by lycopene (5 or 20 mg/kg). Lycopene treatment, especially in the colistin plus lycopene (20 mg/kg) group, significantly downregulated the expression of NF-B mRNA (P < 0.01) but upregulated the expression of nuclear factor erythroid 2-related factor 2 (Nrf2) and HO-1 mRNA (both P < 0.01) in the kidney compared with the results seen with the colistin group. Our data demonstrated that coadministration of 20 mg/kg/day lycopene can protect against colistin-induced nephrotoxicity in mice. This effect may be attributed to the antioxidative property of lycopene and its ability to activate the Nrf2/HO-1 pathway.

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Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

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Lycopene Attenuates Colistin-Induced Nephrotoxicity in Mice via Activation of the Nrf2/HO-1 Pathway

Dai

Tang

Deng

et al. 2015

Antimicrob Agents Chemother

107

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“…It is an important biological free radical scavenger, which can exert its effect both on cells and membranes by protecting low-density lipoproteins and polyunsaturated fats in membranes from oxidation 49 . Authors have shown the effect of vitamin E against gentamicin 14,16,50 , vancomicin 51 , cisplatin 52 and colistin 53 . In the literature, there was no investigation about the effect of vitamin E against AK induced nephrotoxicity in rats.…”

Section: Discussionmentioning

confidence: 99%

Amikacin induced renal damage and the role of the antioxidants on neonatal rats

et al. 2016

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Amikacin (AK) is frequently used on the treatment of Gram-negative infections on neonates, but its usage is restricted because of nephrotoxicity. In this study, on neonatal rats, we aimed to investigate the effects of erythropoietin and vitamin E on AK induced nephrotoxicity. A total of 35 newborn Wistar Albino rats were divided into four groups: (1) injected with saline (serum physiological was administered to placebo controls), (2) injected with AK (1200 mg/kg), (3) injected with AK + vitamin E (150 mg/kg), (4) injected with AK + erythropoietin (EPO) (300 IU/kg/day). In renal tissue, AK levels were significantly high in all groups except the control. Tissue malondialdehyde (MDA) and nitric oxide (NO) levels were statistically higher in AK -treated group than the control. MDA and NO levels were significantly decreased with the administration of vitamin E and EPO. Glutathione peroxidase (GPX) levels were statistically low in AK group compared with the controls. The levels of GPX, in vitamin E group, were increased significantly. However, superoxide dismutase and catalase levels were not significantly different in none of the groups. Insulin-like growth factor-1 values in AK, EPO and vitamin E groups were significantly higher than the control group. Histomorphological changes such as tubular epithelial necrosis were seen in AK treated group. Histopathological improvements observed with EPO and vitamin E administration. AK nephrotoxicity is related to oxidative stress and is supported with biochemical and histopathological findings. Vitamin E and EPO, as antioxidants, can be useful renoprotective agents for ameliorating AK induced nephrotoxicity in neonates.ARTICLE HISTORY

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“…For instance, nephrotoxicity induced by CMS might be due to oxidative damage. The improvement by ATX is related to their antioxidant properties 20 . Pretreatment of ATX is effective in preserving renal function and histology against ischemia/ reperfusion via antioxidant activity 4 .The nephrotoxic effect of cisplatin was diminished by the antioxidant effect of ATX [21].ATX is useful for the prevention of Fe-NTAinduced renal tubular oxidative damage 22 .ATX plays an important role in reduction of oxidative damage and could prevent pathological changes in diabetic rats suggesting promising application of ATX in diabet treatment 23 .…”

Section: Anti-oxidative Effectsmentioning

confidence: 99%

Research Progress of Astaxanthin on Contrast agent induced acute kidney injury

Li¹

2018

J Cardiol and Cardiovasc Sciences

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Contrast agent induced acute kidney injury (CI-AKI) is a leading cause of hospital-acquired acute kidney injury as a result of more and more iodinated contrast-media use for diagnostic purposes. Previous studies have demonstrated that oxidative stress and apoptosis are established processes contributing to contrast agent induced acute kidney injury. Astaxanthin (ATX), a carotenoid found in microalgae, fungi, complex plants, seafood, flamingos and quail has been confirmed have anti-oxidant, and anti-apoptosis effects. Experimental investigations in a range of species using a contrast agent induced acute kidney injury model demonstrated kidney preservation when ATX is administered prior to the induction of contrast agent. ATX, as an natural antioxidant, is capable to prevent CI-AKI effectively, and the mechanism is possibly related to anti-oxidant and anti-apoptosis. In this mini review, we briefly summarize the potential for ATX as a protector against CI-AKI pathologies.

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Evaluation of efficacy of natural astaxanthin and vitamin E in prevention of colistin-induced nephrotoxicity in the rat model

Cited by 58 publications

References 33 publications

Lycopene Attenuates Colistin-Induced Nephrotoxicity in Mice via Activation of the Nrf2/HO-1 Pathway

Lycopene Attenuates Colistin-Induced Nephrotoxicity in Mice via Activation of the Nrf2/HO-1 Pathway

Amikacin induced renal damage and the role of the antioxidants on neonatal rats

Research Progress of Astaxanthin on Contrast agent induced acute kidney injury

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