Selenium Status in Diet Affects Nephrotoxicity Induced by Cisplatin in Mice

Liu, Shuang; Wen, Xing; Huang, Qihan; Zhu, Minghui; Lu, Jun

doi:10.3390/antiox11061141

Cited by 4 publications

(4 citation statements)

References 59 publications

(68 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Selenium has no biological activity of its own, it exerts its effect largely through its presence in the active site of several biologically active selenoproteins [ 13 , 14 , 15 ]. Thus, selenoproteins, as selenium-dependent proteins, are carriers of the biological effects of selenium.…”

Section: Discussionmentioning

confidence: 99%

“…Cells need selenium for many processes, such as the antioxidant process, defense against infection and energy transfer [ 11 , 12 ]. Selenium exerts its effect largely through its presence in the active site of several biologically active selenoproteins [ 13 , 14 , 15 ]. Among them, selenium is best known in the form of glutathione peroxidase-3 (GPX-3), the strongest antioxidant enzyme in the body [ 14 ].…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Effects of Selenium on Chronic Kidney Disease: A Mendelian Randomization Study

Zhang

et al. 2022

Nutrients

View full text Add to dashboard Cite

Background: Previous observational studies have shown that there is a controversial association between selenium levels and chronic kidney disease (CKD). Our aim was to assess the causal relationship between selenium levels and CKD using Mendelian randomization (MR) analysis. Methods: We used the two-sample Mendelian randomization (MR) method to analyze the causal role of selenium levels on CKD risk. The variants associated with selenium levels were extracted from a large genome-wide association study (GWAS) meta-analysis of circulating selenium levels (n = 5477) and toenail selenium levels (n = 4162) in the European population. Outcome data were from the largest GWAS meta-analysis of European-ancestry participants for kidney function to date. Inverse variance weighted (IVW) method was used as the main analysis and a series of sensitivity analyses were carried out to detect potential violations of MR assumptions. Results: The MR analysis results indicate that the genetically predicted selenium levels were associated with decreased estimated glomerular filtration (eGFR) (effect = −0.0042, 95% confidence interval [CI]: −0.0053–0.0031, p = 2.186 × 10−13) and increased blood urea nitrogen (BUN) (effect = 0.0029, 95% confidence interval [CI]: 0.0006–0.0052, p = 0.0136) with no pleiotropy detected. Conclusions: The MR study indicated that an increased level of selenium is a causative factor for kidney function impairment.

show abstract

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Effects of Selenium on Chronic Kidney Disease: A Mendelian Randomization Study

Zhang

et al. 2022

Nutrients

View full text Add to dashboard Cite

show abstract

“…In addition to the oxidative stress implicated in the pathogenesis of cisplatin kidney injury [ 28 , 29 , 30 , 31 , 32 , 33 ], inflammation and renal fibrosis have also been postulated to be involved in cisplatin-induced kidney injury [ 34 , 35 , 36 , 37 , 38 , 39 ]. Cisplatin-induced kidney injury may also involve NAD + redox signaling pathways such as sirt3 [ 40 ], poly-ADP ribosylase (PARP) [ 41 ], and mitochondrial dynamics [ 18 ] including mitochondrial fission and fusion [ 42 , 43 , 44 ].…”

Section: Major Molecular Mechanisms Of Cisplatin-induced Kidney Injurymentioning

confidence: 99%

“…Targeting NAD + redox balance has been suggested as a strategy for fighting cisplatin-induced kidney injury [ 18 , 60 ]. Therefore, there has been an increasing interest in studying redox biochemistry and NAD + redox signaling in the pathogenesis of cisplatin renal toxicity [ 32 , 61 , 62 , 63 , 64 ]. The major NAD + -dependent redox enzymes that may be involved in cisplatin-induced kidney injury are shown in Figure 4 .…”

Section: Effects Of Cisplatin On Major Individual Nad + ...mentioning

confidence: 99%

Cisplatin-Induced Kidney Toxicity: Potential Roles of Major NAD+-Dependent Enzymes and Plant-Derived Natural Products

Iskander

2022

Biomolecules

View full text Add to dashboard Cite

Cisplatin is an FDA approved anti-cancer drug that is widely used for the treatment of a variety of solid tumors. However, the severe adverse effects of cisplatin, particularly kidney toxicity, restrict its clinical and medication applications. The major mechanisms of cisplatin-induced renal toxicity involve oxidative stress, inflammation, and renal fibrosis, which are covered in this short review. In particular, we review the underlying mechanisms of cisplatin kidney injury in the context of NAD+-dependent redox enzymes including mitochondrial complex I, NAD kinase, CD38, sirtuins, poly-ADP ribosylase polymerase, and nicotinamide nucleotide transhydrogenase (NNT) and their potential contributing roles in the amelioration of cisplatin-induced kidney injury conferred by natural products derived from plants. We also cover general procedures used to create animal models of cisplatin-induced kidney injury involving mice and rats. We highlight the fact that more studies will be needed to dissect the role of each NAD+-dependent redox enzyme and its involvement in modulating cisplatin-induced kidney injury, in conjunction with intensive research in NAD+ redox biology and the protective effects of natural products against cisplatin-induced kidney injury.

show abstract

Investigation of the protective effect of selenium supplementation on renal function in cisplatin-administered rats

Altunkaya,

Abuşoğlu,

Ozturk

2024

Cukurova Medical Journal

View full text Add to dashboard Cite

Purpose: Selenium is an important antioxidant and anticarcinogen with the ability to protect cells from oxidative stress, a significant marker of cisplatin-induced toxicity. This study aimed to reveal the effect of selenium on free radicals in cisplatin-induced nephrotoxicity by examining changes in creatinine, neutrophil gelatinase-associated lipocalin (NGAL), and galectin-3, which are associated with kidney damage. Materials and Methods: Twenty-four Wistar albino rats, aged 60 days, were equally divided into four groups: control, cisplatin, selenium, and cisplatin+selenium. The experiment started on the 39th day after the rats were born. Controls were intraperitoneally administered a single dose of physiological saline. Rats in the selenium and cisplatin+selenium groups were administered 1 mg/kg of selenium by gastric gavage per day for 21 days. The rats in the cisplatin and cisplatin+selenium groups were intraperitoneally administered 7.5 mg/kg of cisplatin on the 57th day. The experiment was terminated 3 days after single-dose administration. Tissue samples were analyzed using the ICP-MS method for selenium, the biochemical method for plasma creatinine, and the ELISA method for NGAL and galectin-3. Results: Kidney tissue selenium levels were significantly higher in the selenium-supplemented groups (control;146.8 ± 10.8 ng/dl, selenium;520.2 ± 31.2 ng/dl, cisplatin;140 ± 6.4 ng/dl; cisplatin + selenium; 363.4 ± 33.6 ng/dl). Plasma creatinine levels were statistically significantly higher in the cisplatin-administered groups (control; 0.32 ± 0.01 mg/dl, selenium; 0.32 ± 0.01 mg/dl, cisplatin; 0.47 ± 0.02 mg/dl; cisplatin + selenium; 0.45 ± 0.04). There was no difference in kidney tissue NGAL levels; however, galectin-3 levels were significantly increased in the cisplatin group compared with the other groups. This increase was lower in the cisplatin+selenium group than in the cisplatin group. Heart tissue NGAL and galectin-3 levels were higher in the cisplatin group. Conclusion: Selenium supplementation may have a healing effect on the nephrotoxicity and cardiotoxicity caused by cisplatin, as indicated by changes in creatinine, NGAL, and galectin-3 levels.

show abstract

Selenium Status in Diet Affects Nephrotoxicity Induced by Cisplatin in Mice

Cited by 4 publications

References 59 publications

Effects of Selenium on Chronic Kidney Disease: A Mendelian Randomization Study

Effects of Selenium on Chronic Kidney Disease: A Mendelian Randomization Study

Cisplatin-Induced Kidney Toxicity: Potential Roles of Major NAD+-Dependent Enzymes and Plant-Derived Natural Products

Investigation of the protective effect of selenium supplementation on renal function in cisplatin-administered rats

Contact Info

Product

Resources

About