Protective effect of selenium on aluminium-induced oxidative stress in mouse liver in vivo

Vieželienė, Dalė; Jansen, Eugène; Rodovičius, Hiliaras; Kašauskas, Artūras; Ivanov, Leonid

doi:10.1016/j.etap.2010.11.008

Cited by 32 publications

(20 citation statements)

References 23 publications

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“…Repeated ip injections reduced GSH and GST and increased LPO in proximal tubule cells. These cells developed toxicity consistent with oxidative damage induced by Al +3 as seen in other studies (Bhaduria 2012, Kaneko et al 2004, Viezeliene et al 2011, 2012). …”

Section: Renalsupporting

confidence: 87%

“…In a series of studies by Viezeliene et al (2011, 2012) concerning potential amelioration of Al—induced liver damage by selenite, BALB/C mice were given ip injections of 25 mg/kg AlCl 3 and 1.25 mg/kg Na 2 SeO 3 ; selenite injection was made 20 min prior to administration of AlCl 3 . At 16-h post-injection there was an increase in hepatic protein synthesis and serum ALT, but Na 2 SeO 3 injection alone had no influence on ALT.…”

Section: Hepaticmentioning

confidence: 99%

“…The authors interpreted these changes as indicative of Al-induced oxidative stress in mouse hepatocytes secondary to Al disruption of hepatocyte membranes and/or interference with PO 4 and ATP generation. Limitations to the Viezeliene et al (2011, 2012) reports include the absence of dose-response descriptions and measures of Al and Se in blood or liver.…”

Section: Hepaticmentioning

confidence: 99%

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Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Willhite¹,

Karyakina²,

Yokel³

et al. 2014

Critical Reviews in Toxicology

329

201

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Aluminum (Al) is a ubiquitous substance encountered both naturally (as the third most abundant element) and intentionally (used in water, foods, pharmaceuticals, and vaccines); it is also present in ambient and occupational airborne particulates. Existing data underscore the importance of Al physical and chemical forms in relation to its uptake, accumulation, and systemic bioavailability.Address for correspondence: Calvin C. Willhite, Risk Sciences International, 55 Metcalfe Street, Suite 700, Ottawa, ON, Canada. calvinwillhite@hotmail.com. Declaration of interestPartial funding for this work was provided by a contract to review the recent scientific literature on health effects of aluminum between the International Aluminium Institute (IAI, www.world-aluminium.org), the Aluminium Reach Consortium (ARC, www.aluminium-reach-consortium.eu), and Risk Sciences International (RSI, www.risksciences.com), a Canadian company established in 2006 in partnership with the University of Ottawa. Additional financial support was provided by the Natural Sciences and Engineering Research Council of Canada (NSERC) to D. Krewski, who holds the NSERC Chair in Risk Science at the University of Ottawa. C.C. Willhite, N.A. Karyakina, F. Momoli, and N. Yenugadhati were compensated by RSI for their contributions to the review. I. Arnold, T. Wisniewski and R. Yokel received no compensation from RSI for their contributions to this work. The authors, whose affiliations are shown on the title page, had sole responsibility for preparation of this paper, including determining the strategy for reviewing the scientific literature summarized in this article, synthesizing the findings, and drawing conclusions. Scientists associated with IAI/ARC were given the opportunity to review and offer technical comments on the paper, prior to submission to Critical Reviews in Toxicology. I. Arnold serves as a consultant to the International Aluminium Institute. None of the authors have appeared before regulatory agencies on behalf of the sponsors, or appeared as experts in legal proceedings concerning matters reviewed in this paper. The scientific opinions and conclusions expressed in the paper are exclusively those of the authors, and are independent of the sources of financial support. HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptThe present review represents a systematic examination of the peer-reviewed literature on the adverse health effects of Al materials published since a previous critical evaluation compiled by Krewski et al. (2007). The scientific literature on the adverse health effects of Al is extensive. Health risk assessments for Al must take into account individual co-factors (e.g., age, renal function, diet, gastric pH). Conclusions from the current review point to the need for refinement of the PTWI, reduction of Al contamination in PN solutions, justification for routine addition of Al to vaccines, and harmonization of OELs for Al substances.

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Section: Renalsupporting

confidence: 87%

Section: Hepaticmentioning

confidence: 99%

Section: Hepaticmentioning

confidence: 99%

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Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Willhite¹,

Karyakina²,

Yokel³

et al. 2014

Critical Reviews in Toxicology

329

201

View full text Add to dashboard Cite

show abstract

“…Визначали активність глутатіонпероксидази (1.11.1.9), глутатіонредуктази (1.8.1.7) та су-пероксиддисмутази (1.15.1.1) в еритроци-тах із застосуванням комерційних наборів Randox та Ransod (Randox Laboratories Ltd, Велика Британія). Вміст загального глутатіону в еритроцитах визначали після відновлення окисленого глутатіону за допомо-гою глутатіонредуктази шляхом його реакції з 5,5′-дитіобіс-2-нітробензойною кислотою, а вміст окисленого глутатіону -аналогічним шляхом, але після інактивації відновленого глутатіону 2-вінілпіридином [69].…”

Section: в огляді узагальнено дані літератури і результати власних доunclassified

Biological role of fetuin a and its potential importance for prediction of cardiovascular risk in patients with type 2 diabetes mellitus

Gorshunska¹

2013

Ukr.Biochem.J.

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“…9 Se plays an important role in a number of physiological processes, including the neutralization of reactive oxygen species (ROS) and the modulation of redox-sensitive enzyme cascades. 10,11 Recently, Trabelsi et al demonstrated that subacute exposure to cadmium (Cd) generates nanocomplexes (CdS and/or CdSe) at cellular levels in the liver and kidneys. 12,13 The authors reported that Se decreases the oxidative responses by enhancing the biosynthesis of nanocomplexes (CdSe and/or CdS) in rat nephrocytes.…”

Section: Introductionmentioning

confidence: 99%

Interaction between nanoparticles generated by zinc chloride treatment and oxidative responses in rat liver

Azzouz¹,

Trabelsi²,

Hanini³

et al. 2013

IJN

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The aim of the present study was to investigate the interaction of zinc chloride (3 mg/kg, intraperitoneally [ip]) in rat liver in terms of the biosynthesis of nanoparticles. Zinc treatment increased zinc content in rat liver. Analysis of fluorescence revealed the presence of red fluorescence in the liver following zinc treatment. Interestingly, the co-exposure to zinc (3 mg/kg, ip) and selenium (0.20 mg/L, per os [by mouth]) led to a higher intensity of red fluorescence compared to zinc-treated rats. In addition, X-ray diffraction measurements carried out on liver fractions of zinc-treated rats point to the biosynthesis of zinc sulfide and/or selenide nanocomplexes at nearly 51.60 nm in size. Moreover, co-exposure led to nanocomplexes of about 72.60 nm in size. The interaction of zinc with other mineral elements (S, Se) generates several nanocomplexes, such as ZnS and/or ZnSe. The nanocomplex ZnX could interact directly with enzyme activity or indirectly by the disruption of mineral elements’ bioavailability in cells. Subacute zinc or selenium treatment decreased malondialdehyde levels, indicating a drop in lipid peroxidation. In addition, antioxidant enzyme assays showed that treatment with zinc or co-treatment with zinc and selenium increased the activities of glutathione peroxidase, catalase, and superoxide dismutase. Consequently, zinc complexation with sulfur and/or selenium at nanoscale level could enhance antioxidative responses, which is correlated to the ratio of number of ZnX nanoparticles (X=sulfur or X=selenium) to malondialdehyde level in rat liver.

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Protective effect of selenium on aluminium-induced oxidative stress in mouse liver in vivo

Cited by 32 publications

References 23 publications

Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Systematic review of potential health risks posed by pharmaceutical, occupational and consumer exposures to metallic and nanoscale aluminum, aluminum oxides, aluminum hydroxide and its soluble salts

Biological role of fetuin a and its potential importance for prediction of cardiovascular risk in patients with type 2 diabetes mellitus

Interaction between nanoparticles generated by zinc chloride treatment and oxidative responses in rat liver

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