Vitamin E Is a Nephroprotectant Agent in Male but Not in Female in a Model of Cisplatin-Induced Nephrotoxicity

Jilanchi, Sima; Nematbakhsh, Mehdi; Bahadorani, Mehrnoosh; Talebi, Ardeshir; Eshraghi-Jazi, Fatemeh; Azam, Mahalul; Ashrafi, Farzaneh

doi:10.5402/2013/280395

Cited by 21 publications

(24 citation statements)

References 39 publications

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“…Additionally, another similar study, researcher confirmed that administration of vitamin E (1 g/kg/d) for 7 days prevented cisplatin‐induced nephrotoxicity just in male rats. After vitamin E administration to each gender of Wistar rats received a single dose of cisplatin (7 mg/kg; IP), it was found that although the serum levels of blood urea and creatinine in male cisplatin‐treated animals was not different from the control group, it was significantly different in the female rats ( P < 0.05) …”

Section: Resultsmentioning

confidence: 99%

“…The potential protective effects of vitamin E administration, alone or in combination with other agents have been assessed in several clinical or preclinical studies . For example, Varzi et al demonstrated that vitamin E in combination with silymarin could ameliorate the nephrotoxicity induced by gentamicin at a dosage of 20 mg/kg, once daily for 9 days, in dogs.…”

Section: Introductionmentioning

confidence: 99%

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Has vitamin E any shreds of evidence in cisplatin‐induced toxicity

Hakiminia

Goudarzi²,

Moghaddas

2019

J Biochem & Molecular Tox

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Cisplatin is one of the highly consumed and effective antitumor agents whose clinical application is accompanied by nephrotoxicity adverse reaction. Also, other complications such as ototoxicity and hepatotoxicity are a matter of concern. Today, it is suggested that cisplatin‐associated toxicities are mainly induced by free radicals production, which will result in oxidative organ injury. The evidence is growing over the protective effects of antioxidants on cisplatin‐induced adverse reactions especially nephrotoxicity. The possible protective effects of vitamin E and its derivative in cisplatin‐induced nephrotoxicity and ototoxicity are reviewed here at the light of pertinent results from basic and clinical research. Administration of vitamin E alone or in combination with other antioxidant agents could cause amelioration in oxidative stress biomarkers such as decreasing the level of malondialdehyde, reducing serum urea and creatinine, and also enhancing the activities of renal antioxidant enzymes including renal catalase, glutathione‐S‐transferase, and superoxide dismutase. Although the data from most of the studies are in favors of protective effects of vitamin E against cisplatin‐induced toxicity, more clinical trials are needed to clarify the clinical importance of vitamin E administration as an antioxidant during cisplatin therapy in cancer condition.

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Section: Resultsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Has vitamin E any shreds of evidence in cisplatin‐induced toxicity

Hakiminia

Goudarzi²,

Moghaddas

2019

J Biochem & Molecular Tox

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“…They have also reported that the vasodilator effect of NO improves the blood flow which can, in its own turn, decrease tissue damage (24). In another study, Jilanchi et al have shown that, in cisplatin nephrotoxicity, vitamin E modified BUN and Cr level in male rates; while this effect was not observed in female rats (22). Actually, antioxidant vitamins act as free radical scavengers, therefore, the decrease of kidney damage can improve BUN and Cr level.…”

Section: Discussionmentioning

confidence: 98%

“…The first and second groups, each including nine rats, received gentamicin (80 mg/kg/d) for 9 days (21). Similarly, the third and fourth groups, each including nine rats, received a regular dose of gentamicin (80 mg/kg/d) + vitamin E (1 g/kg/d) for 9 days (22). The fifth and sixth groups, each consisting of eight animals, obtained a continuous dose of gentamicin (80 mg/kg/d) + vitamin C (250 mg/kg/d) for 9 days (23).…”

Section: Experimental Protocolmentioning

confidence: 99%

Nitric oxide metabolite changes in gentamicin-induced nephrotoxicity; the effects of antioxidant vitamins

Safari¹,

Miri²,

Gharaei³

et al. 2017

J Renal Inj Prev

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In this experimental study, 68 adult Wistar rats made the subject of the study. Administration of vitamin E and C, in an individual manner, can have some more favorable effects on urea, creatinine and nitrite level in GM nephrotoxicity than their coadministration. On the other hand, there is a gender difference, in response to vitamin E and C in which male gender responded more favorably to the antioxidant vitamins.

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“…However, detrimental changes in NRCM secondary to higher levels of ROS cannot be prevented, as reflected by the findings in the post-treatment group (Jilanchi et al, 2013). As with this study, the oxidative damage occurring after H 2 O 2 induction most probably could not be repaired by TRF, hence giving rise to progressive cell death (Han et al, 2004).…”

Section: Discussionmentioning

confidence: 47%

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Supplemental Information 1: Raw Data

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Background: Oxidative stress plays an important role in the pathogenesis of heart diseases. Antioxidants such as palm tocotrienol-rich fraction (TRF) can reduce oxidative stress, hence preventing and reducing the risk of heart disease. This study was aimed to determine the protective effects of TRF against hydrogen peroxide (H 2 O 2)-induced oxidative stress in neonatal rat cardiomyocytes (NRCM). Methods: The NRCM were divided into five groups: (1) control, (2) cells treated with TRF (10 µg/ml) for 24 hours, (3) cells subjected to H 2 O 2 (0.5 mM) for 30 minutes, (4) cells pre-treated with TRF, and (5) cells post-treated with TRF. The IC 50 of H 2 O 2 (0-5 mM) and the effective dose of TRF (0-25 µg/ml) were determined using the MTS cell viability assay. Meanwhile, ELISA was used to measure the level of reactive oxygen species (ROS). The presence of superoxides and H 2 O 2 were detected by dihydroethidium and 5-(and-6)-carboxy-2′,7′dichlorodihydrofluorescein diacetate respectively. Flowcytometry analysis was conducted to determine the presence of apoptosis and measure the mitochondrial membrane potential, whereby the former involved the use of Annexin V-FITC stain while the latter JC-1 stain. The gene expressions of antioxidant (SOD, CAT, GPx) and apoptosis (Bax, Bcl-2, Caspase-3) enzymes were studied using qRT-PCR. Results: The IC 50 of H 2 O 2 was 0.5 mM while the effective dose of TRF 10 µg/ml. The cells which were subjected to H 2 O 2 showed a decrease in NRCM viability and significant increase (p < 0.05) in ROS production. LDH activity and green fluorescence intensity (which indicated mitochondrial depolarisation) were increased following H 2 O 2 induction. With reference to the control, the H 2 O 2-induced group had a higher percentage of late apoptotic cells, which was associated with the upregulation of the pro-apoptotic gene, Bax, and downregulation of the anti-apoptotic gene, Bcl-2 (p < 0.05). H 2 O 2 also upregulated GPx expression , apart from downregulating CAT and Cu/Zn SOD expression (p < 0.05). The pre-and post-treatment groups had increased cell viability and reduced ROS production. Pre-treatment with TRF protected the cell membranes and mitochondria from H 2 O 2-induced injury, as reflected by the reduction in extracellular LDH activity and apoptosis (the latter of which was associated with the

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Vitamin E Is a Nephroprotectant Agent in Male but Not in Female in a Model of Cisplatin-Induced Nephrotoxicity

Cited by 21 publications

References 39 publications

Has vitamin E any shreds of evidence in cisplatin‐induced toxicity

Has vitamin E any shreds of evidence in cisplatin‐induced toxicity

Nitric oxide metabolite changes in gentamicin-induced nephrotoxicity; the effects of antioxidant vitamins

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