Organic silicon protects human neuroblastoma SH-SY5Y cells against hydrogen peroxide effects

BMC Complementary and Alternative Medicine

Juana Benedí²  Sara Bastida³  Francisco J Sánchez-Muniz³  Maria Isabel Sánchez-Reus¹  Maria Pilar González¹  José J Merino¹  Alba Garcimartín³ 

[1] Departamento de Bioquímica y Biología Molecular II, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain;Depatamento de Farmacología, Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain;Departamento de Nutrición y Bromatología I (Nutrición), Facultad de Farmacia, Universidad Complutense de Madrid, 28040 Madrid, Spain

关键词: Neuroprotection;    Caspase-3,-8,-9;    ROS;    LDH;    Cellular death;    Silicon;   

Others  :  1086291
DOI  :  10.1186/1472-6882-14-384

 received in 2014-06-30, accepted in 2014-09-29,  发布年份 2014

【 摘 要 】

Background

Hydrogen peroxide (H₂O₂) is a toxic agent that induces oxidative stress and cell death. Silicon (Si) is a biological element involved in limiting aluminium (Al) absorption with possible preventive effects in Alzheimer’s disease. However, Si has not yet been associated with other neuroprotective mechanisms.

Methods

The present experiments evaluated in the SH-SY5Y human neuroblastoma cell line the possible role of different Si G5 (50-1000 ng/mL) concentrations in preventing cellular death induced by H₂O₂ (400 μM, 24 hours).

Results

Our findings showed that H₂O₂ promoted cell death in the human SH-SY5Y cell cultures and this could be prevented by Si treatment. The loss in cell viability mediated by H₂O₂ was due to an apoptotic and necrotic process. Apoptotic death was incurred by regulating caspase-8 activity in the extrinsic pathway. The apoptotic and necrotic cell death induced by H₂O₂ was almost totally reversed by Si (50-500 ng/mL), indicating that it down-regulates both processes in H₂O₂ treated cells.

Conclusions

According to our data, Si is able to increase SH-SY5Y cell survival throughout partially blocking cellular damage related to oxidative stress through a mechanism that would affect H₂O₂/ROS elimination.

【 授权许可】

   
2014 Garcimartín et al.; licensee BioMed Central Ltd.

【 图 表 】

Figure 1.

Figure 2.

Figure 3.

Figure 4.

Figure 5.

Figure 6.

Figure 7.

【 参考文献 】

• [1]Edwardson JA, Moore PB, Ferrier IN, Lilley JS, Newton GW, Barker J, Templar J, Day JP: Effect of silicon on gastrointestinal absorption of aluminum. Lancet 1993, 342:211-212.
• [2]Carlisle EM, Curran MJ: Effect of dietary silicon and aluminum on silicon and aluminum levels in rat brain. Alzheimer Dis Assoc Disord 1987, 1:83-89.
• [3]Bellès M, Sanchez DJ, Gómez M, Corbella J, Domingo JL: Silicon reduces aluminum accumulation in rats: relevance to the aluminum hypothesis of Alzheimer’s disease. Alzheimer Dis Assoc Disord 1998, 12:83-87.
• [4]Greenwood NN, Earnshaw A: Chemistry of the Elements. 2nd edition. Oxford: Butterworth-Heinemann; 1997.
• [5]Carlisle EM: Silicon: an essential element for the chick. Science 1972, 178:619-621.
• [6]Schwarz K, Milne DB: Growth promoting effects of silicon in rats. Nature 1972, 239:333-334.
• [7]Candy JM, Edwardson JA, Klinowski J, Oakley AE, Perry EK, Perry RH: Colocalisation of Aluminum and Silicon in Senile Plaques: Implications for the Neurochemical Pathology of Alzheimer’s Disease. In Senile Dementia of the Alzheimer Type. Edited by Traber J, Gispen WH. Heidelberg: Springer; 1985:183-197.
• [8]Jurkić LM, Cepanec I, Pavelić KS, Pavelić K: Biological and therapeutic effects of ortho-silicic acid and some ortho-silicic acid-releasing compounds: new perspectives for therapy. Nutr Metab 2013, 10:1-12. BioMed Central Full Text
• [9]Dobbie JW, Smith MJB: The silicon content of body fluids. Scott Med J 1982, 27:17-19.
• [10]Dobbie JW, Smith MJB: Silicon: its role in medicine and biology. Scott Med J 1982, 27:1-2.
• [11]D’Haese PC, Shaheen FA, Huraib SO, Djukanovic L, Polenakovic MH, Spasovski G, Shikole A, Schurgers ML, Daneels RF, Lamberts LV, Van Landeghem GF, De Broe ME: Increased silicon levels in dialysis patients due to high silicon content in the drinking water, inadequate water treatment procedures, and concentrate contamination: a multicentre study. Nephrol Dial Transplant 1995, 10:1838-1844.
• [12]Perry CC, Keeling-Tucker T: Aspects of the bioinorganic chemistry of silicon in conjunction with the biometals calcium, iron and aluminium. J Inorg Biochem 1998, 69:181-191.
• [13]Exley C: Darwin, natural selection and the biological essentiality of aluminium and silicon. Trends Biochem Sci 2009, 34:589-593.
• [14]Scientific Committee for Food: Nutrient and Energy Intakes for the European Community. Luxembourg: European Commission; 1993. [Reports of the Scientific Committee for Food (Thirty-first series)]
• [15]European Food Safety Authority: Opinion of the scientific panel on dietetic products, nutrition and allergies on a request from the commission related to the tolerable upper intake level of silicon. EFSA J 2004, 60:1-11.
• [16]Van Dyck K, Robberecht H, Van Cauwenbergh R, Van Vlaslaer V, Deelstra H: Indication of silicon essentiality in humans. serum concentrations in Belgian children and adults including pregnant women. Biol Trace Elem Res 2000, 77:25-32.
• [17]Bissé E, Epting T, Beil A, Lindinger G, Lang H, Wieland H: Reference values for serum silicon in adults. Anal Biochem 2005, 337:130-135.
• [18]González-Muñoz MJ, Meseguer I, Sanchez-Reus MI, Schultz A, Olivero R, Benedi J, Sánchez-Muniz FJ: Beer consumption reduces cerebral oxidation caused by aluminum toxicity by normalizing gene expresión of tumor necrotic alpha and several antioxidant enzymes. Food Chem Toxicol 2008, 46:1111-1118.
• [19]Candy JM, Oakley AE, Klinowski J, Carpenter TA, Perry EK, Blessed G, Fairbairn A, Edwardson JA: Aluminosilicates and senile plaque formation in Alzheimer’s disease. Lancet 1986, 1:354-357.
• [20]Davenward S, Bentham P, Wright J, Crome P, Job D, Polwart A, Exley C: Silicon-rich mineral water as a non-invasive test of the ‘aluminum hypothesis’ in Alzheimer’s disease. J Alzheimers Dis 2013, 33:423-430.
• [21]Miu AC: The silicon link between aluminium and Alzheimer’s disease. J Alzheimers Dis 2006, 10:39-42.
• [22]Rondeau V, Jacqmin-Gadda H, Commenges D, Helmer C, Dartigues JF: Aluminum and Silica in drinking water and the risk of Alzheimer’s disease or cognitive cecline: findings from 15-year follow-up of the PAQUID cohort. Am J Epidemiol 2009, 169:489-496.
• [23]Kress M, Ried B, Reeh PW: Effects of oxygen radicals on nociceptive afferents in the rat skin in vitro. Pain 1995, 62:87-94.
• [24]Waldron RT, Rozengurt E: Oxidative stress induces protein kinase D activation in intact cells. involvement of Src and dependence on protein kinase C. J Biol Chem 2000, 275:17114-17121.
• [25]Bayani AA: Psychometric data for a Farsi translation of the Trait Meta-Mood Scale. Psychol Rep 2009, 105:198-204.
• [26]Bradford MA: Rapid sensitive method for the quantitation of microgram quantities of protein utilizing the principle of protein-dye binding. Anal Biochem 1976, 72:248-254.
• [27]López E, Figueroa S, Oset-Gasque MJ, González MP: Apoptosis and necrosis: two distinct events induced by cadmium in cortical neurons in culture. Br J Pharmacol 2003, 138:901-911.
• [28]Mihara M, Uchiyama M: Determination of malonaldehyde precursor in tissues by thiobarbituric acid test. Anal Biochem 1978, 86:271-278.
• [29]Nagai N, Ito Y: Excessive hydrogen peroxide enhances the attachment of amyloid β1-42 in the lens epithelium of UPL rats, a hereditary model for cataracts. Toxicology 2014, 315:55-64.
• [30]Xie H, Hou S, Jiang J, Sekutowicz M, Nelly J, Bacskai BJ: Rapid cell death is precede by amyloid plaque-mediated oxidative stress. Proc Natl Acad Sci U S A 2013, 110:7904-7909.
• [31]Chetsawang J, Govitrapong P, Chetsawang B: Hydrogen peroxide toxicity induces ras signaling in human neuroblastoma SH-SY5Y cultured cells. J Biomed Biotechnol 2010, 2010:803815.
• [32]Steenland K, Ward E: Silica: a lung carcinogen. CA Cancer J Clin 2014, 64:63-69.
• [33]Zhou T, Rong Y, Liu Y, Zhou Y, Guo J, Cheng W, Wang H, Chen W: Association between proinflammatory responses of respirable silica dust and adverse health effects among dust-exposed workers. J Occup Environ Med 2012, 54:459-465.
• [34]Valencia A, Moran J: Reactive oxygen species induce different cell death mechanisms in cultured neurons. Free Radic Biol Med 2004, 36:1112-1125.
• [35]Fatokun AA, Stone TW, Smith RA: Adenosine receptor ligands protect against a combination of apoptotic and necrotic cell death in cerebellar granule neurons. Exp Brain Res 2008, 186:151-160.
• [36]Uttara B, Singh AV, Zamboni P, Mahajan RT: Oxidative stress and neurodegenerative diseases: a review of upstream and downstream antioxidant therapeutic options. Curr Neuropharmacol 2009, 7:65-74.
• [37]Jenner P: Oxidative stress in Parkinson’s disease. Ann Neurol 2003, 53:S26-S36.
• [38]Pratico D: Evidence of oxidative stress in Alzheimer’s disease brain and antioxidant therapy. Ann N Y Acad Sci 2008, 1147:70-78.
• [39]Allen CL, Bayraktutan U: Oxidative stress and its role in the pathogenesis of ischemic stroke. Int J Stroke 2009, 4:461-470.
• [40]Merino JJ, Oset-Gasque MJ: The CXCR7 activation by SDF1 induces neural progenitor migration (NPC): a dual effect on CXCR4/CXCR7 axis within the vascular niche of ischemic rats. Int J Stroke 2013, 8:E56.
• [41]Ryter SW, Kim HP, Hoetzel A, Park JW, Nakahira K, Wang X, Choi AM: Mechanisms of cell death in oxidative stress. Antioxid Redox Signal 2000, 9:49-89.
• [42]Samuilov VD, Kiselevsky DB, Shestak AA, Nesov AV, Vasil’ev LA: Reactive oxygen species in programmed death of pea guard cells. Biochem-Moscow 2008, 73:1076-1084.
• [43]Sun B, Sun GB, Xiao J, Chen RC, Wang X, Wu Y, Cao L, Yang ZH, Sun XB: Isorhamnetin inhibits H2O2-induced activation of the intrinsic apoptotic pathway in H9c2 cardiomyocytes through scavenging reactive oxygen species and ERK inactivation. J Cell Biochem 2012, 113:473-485.
• [44]Sui XQ, Xu ZM, Xie MB, Pei DA: Resveratrol inhibits hydrogen peroxide-induced apoptosis in endothelial cells via the activation of PI3K/Akt by miR-126. J Atheroscrerosc Thromb 2014, 21:108-118.
• [45]Okahashi N, Nakata M, Sumitomo T, Terao Y, Kawabata S: Hydrogen peroxide produced by oral Streptococci induces macrophage cell death. PLoS One 2013, 8:1-6.
• [46]Medan D, Wang L, Toledo D, Lu B, Stehlik C, Shi X, Rojanasakul Y: Regulation of Fas (CD95/ APO-1)-mediated apoptosis and necrosis by reactive oxygen species in macrophages. J Cell Physiol 2005, 203:78-84.
• [47]Wang L, Azad N, Kongkaneramit L, Chen F, Lu Y, Jiang BH, Rojanasakul Y: The Fas death signalling pathway connecting reactive oxygen species generation and FLICE inhibitory protein down-regulation. J Immunol 2008, 180:3072-3080.