Serum selenium levels are associated with age-related cataract
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2nd Department of Ophthalmology, Pomeranian Medical University, Szczecin, Poland
Department of Genetics and Pathomorphology, Pomeranian Medical University, Szczecin, Poland
1st Department of Ophthalmology, Pomeranian Medical University, Szczecin, Poland
Wojciech Lubiński   

2nd Department of Ophthalmology, Pomeranian Medical University in Szczecin
Ann Agric Environ Med. 2018;25(3):443–448
The aim of the study is to analyse correlations between age-related cataract (ARC), serum selenium levels and glutathione peroxidase gene 1 and 4 (GPX-1 and GPX-4).

Material and methods:
A total sample of 275 participants were enrolled into the study: group A, 94 subjects elligible for ARC surgery, and group B, 181 volunteers without ocular symptoms, gender-, age-, and smoking- status and volume-matched at 1:2 with subjects in group A. All participants (n=275) were divided according to the Lens Opacities Classification System III (LOCS III) into: 1) study group (subjects with clinically significant cataract; N≥3 or C≥3 or P≥2), 2) control group (controls with clinically non-significant cataract; N<3 and C<3 and P<2). The single nucleotide polymorphisms of GPX-1 and GPX-4 were assessed using Real Time PCR. Serum selenium levels were assayed using Inductively Coupled Plasma Mass Spectrometry.

Low selenium levels significantly predicted any age-related cataract (OR 7.969; p<.01), nuclear cataract (OR 12.823; p<.01) and cortical cataract (OR 3.31; p<.01). There was no significant effect of gender, age, SNP GPX-1 and SNP GPX-4 on the prevalence of age-related nuclear, cortical and posterior sub-capsular cataract. Serum selenium levels of 75–85 µg/L were associated with the lowest prevalence of ARC.

Due to a confirmed association between serum selenium levels and age-related cataract, low serum selenium levels may constitute a potential risk factor of age-related cataract.

Collective work. Prevention of Blindness and Visual Impairment, World Health Organization website Accessed 30th June 2017.
Schein OD, Cassard SD, Tielsch JM, Gower EW. Cataract surgery among Medicare beneficiaries. Ophthalmic Epidemiol. 2012; 19: 257-64.
Collective work. Lens and Cataract. San Fransisco, American Academy of Ophthalmology, 2015; 65.
Truscott RJ, Friedrich MG. The etiology of human age-related cataract. Proteins don't last forever. Biochem Biophys Acta. 2016; 1860: 192-8.
Shiels A, Hejtmancik JF. Molecular Genetics of Cataract. Prog Mol Biol Transl Sci. 2015; 134: 203-18.
Petrash JM. Aging and age-related diseases of the ocular lens and vitreous body. Invest Ophthalmol Vis Sci. 2013; 54: 54-9.
Akpek EK, Smith RA. Current treatment strategies for age-related ocular conditions. Am J Manag Care. 2013; 19: 76-84.
Beebe DC, Holekamp NM, Shui YB. Oxidative damage and the prevention of age-related cataracts. Ophthalmic Res. 2010; 44: 155-65.
Michael R, Bron AJ. The ageing lens and cataract: a model of normal and pathological ageing. Philos Trans R Soc Lond B Biol Sci. 2011; 1568: 1278-92.
Ganea E, Harding JJ. Glutathione-related enzymes and the eye. Curr Eye Res. 2006; 31: 1-11.
Truscott RJ. Age-related nuclear cataract-oxidation is the key. Exp Eye Res. 2005; 80: 709-25.
Arnér ES. Selenoproteins - What unique properties can arise with selenocysteine in place of cysteine? Exp Cell Res. 2010; 316: 1296-303.
Kisić B, Mirić D, Žorić L, Ilić A, Dragojević I. Reduced glutathione level and GSH-dependent enzyme activities in corticonuclear blocks of lenses in patients with senile cataract. Srp Arh Celok Lek. 2012; 140: 563-70.
Miric DJ, Kisic BB, Zoric LD, Mitic RV, Miric BM, Dragojevic IM. Xanthine oxidase and lens oxidative stress markers in diabetic and senile cataract patients. J Diabetes Complications. 2013; 27: 171-6.
Harding JJ. Free and protein bound glutathione in normal and cataractous human lens. Biochem. J. 1970; 117: 957-60.
Rathbun WB, Bovis MG, Holleschau AM. Glutathione peroxidase, glutathione reductase and glutathione-S-transferase activities in the rhesus monkey lens as a function of age. Curr Eye Res. 1986; 5: 195-9.
Rathbun WB, Bovis MG. Activity of glutathione peroxidase and glutathione reductase in the human lens related to age. Curr Eye Res. 2001; 5: 381-5.
Reddy VN, Giblin FJ, Lin LR, et al. Glutathione peroxidase-1 deficiency leads to increased nuclear light scattering, membrane damage, and cataract formation in gene-knockout mice. Invest Ophthalmol Vis Sci. 2001; 42: 3247-55.
Karaküçük S, Ertugrul Mirza G, Faruk Ekinciler O, Saraymen R, Karaküçük I, Ustdal M. Selenium concentrations in serum, lens and aqueous humour of patients with senile cataract. Acta Ophthalmol Scand. 1995; 73: 329-32.
Xing KY, Lou MF. Effect of H2O2 on human lens epithelial cells and the possible mechanism for oxidative damage repair by thioltransferase. Exp Eye Res. 2002; 74: 113-22.
Cai QY, Chen XS, Zhu LZ, et al. Biochemical and morphological changes in the lenses of selenium and/or vitamin E deficient rats. Biomed Environ Sci. 1994; 7: 109–115.
Flohé L Selenium, selenoproteins and vision. Dev Ophthalmol. 2005; 38: 89-102.
Duffield AJ, Thomson CD, Hill KE, Williams S. An estimation of selenium requirements for New Zealanders. Am J Clin Nutr. 1999; 70: 896–903.
Thomson CD, Robinson MF, Butler JA, Whanger PD. Long term supplementation with selenate and selenomethionine:selenium and glutathione peroxidase in blood components of New Zealand women. Br J Nutr. 1993; 69: 577–588.
Combs GF Jr. Selenium in global food systems. Br J Nutr. 2001; 85: 517-47.
Markiewicz-Żukowska Renata Selen w żywności (access: 03/04/2018).
Thomson CD. Assessment of requirements for selenium and adequacy of selenium status: a review. Eur J Clin Nutr. 2004; 58: 391-402.
Lener M, Jaworska K, Muszyńska M, et al. Selenium as marker for cancer risk and prevention. Pol Przegl Chir. 2012; 84: 470–475.
Dawczynski J, Winnefeld K, Königsdörffer E, Augsten R, Blum M, Strobel J. Selenium and cataract-risk factor or useful dietary supplement? Klin Monbl Augenheilkd. 2006; 223: 675-80.
Jablonska E, Gromadzinska J, Reszka E, et al. Association between GPx1 Pro198Leu polymorphism, GPx1 activity and plasma selenium concentration in humans. Eur J Nutr. 2009; 48: 383-6.
Takata Y, King IB, Lampe JW, et al. Genetic variation in GPX1 is associated with GPX1 activity in a comprehensive analysis of genetic variations in selenoenzyme genes and their activity and oxidative stress in humans. J Nutr. 2012; 142: 419-26.
Donadio JL, Guerra-Shinohara EM, Rogero MM, Cozzolino SM. Influence of Gender and SNPs in GPX1 Gene on Biomarkers of Selenium Status in Healthy Brazilians. Nutrients. 2016; 8: 5 doi: 10.3390/nu8050081.
Nirmalan PK, Robin AL, Katz J, et al. Risk factors for age related cataract in a rural population of southern India: the Aravind Comprehensive Eye Study. Br J Ophthalmol. 2004; 88: 989-94.
Oishi N, Morikubo S, Takamura Y, et al. Correlation between adult diabetic cataracts and red blood cell aldose reductase levels. Invest Ophthalmol Vis Sci. 2006; 47: 2061-4.
Raman R, Pal SS, Adams JS, Rani PK, Vaitheeswaran K, Sharma T. Prevalence and risk factors for cataract in diabetes: Sankara Nethralaya Diabetic Retinopathy Epidemiology and Molecular Genetics Study, report no. 17. Invest Ophthalmol Vis Sci. 2010; 51: 6253-61.
Hill KE, Burk RF, Lene JM. Effect of selenium depletion and repletion on plasma glutathione and glutathione dependent enzymes in the rat. J Nutr. 1987; 117: 99–104.
Nakane T, Asayama K, Kodera K, Hayashibe H, Uchida N, Nakazawa S. Effect of selenium deficiency on cellular and extracellular glutathione peroxidases: immunochemical detection and mRNA analysis in rat kidney and serum. Free Radic Biol Med. 1998; 25: 504-11.
Li X, Qu ZC, May JM. GSH is required to recycle ascorbic acid in cultured liver cell lines. Antioxid Redox Signal. 2001; 3: 1089 –1097.
Chan AW, Ho YS, Chung SK, Chung SS. Synergistic effect of osmotic and oxidative stress in slow-developing cataract formation. Exp Eye Res. 2008; 87: 454-61.
Wang H, Gao J, Sun X, et al. The effects of GPX-1 knockout on membrane transport and intracellular homeostasis in the lens. J Membr Biol. 2009; 227: 25-37.
Cheng W, Fu YX, Porres JM, Ross DA, Lei XG. Selenium-dependent cellular glutathione peroxidase protects mice against a pro-oxidant-induced oxidation of NADPH, NADH, lipids, and protein. FASEB J. 1999; 13: 1467-75.
Giblin FJ, Reddy VN. Pyridine nucleotides in ocular tissues as determined by the cycling assay. Exp Eye Res. 1980; 31: 601-9.
Reddy VN, Lin LR, Ho YS, et al. Peroxide-induced damage in lenses of transgenic mice with deficient and elevated levels of glutathione peroxidase. Ophthalmologica. 1997; 211: 192-200.
Mao J, Vanderlelie JJ, Perkins AV, Redman CW, Ahmadi KR, Rayman MP. Genetic polymorphisms that affect selenium status and response to selenium supplementation in United Kingdom pregnant women. Am J Clin Nutr. 2016; 103: 100-6.
Knekt P, Heliovaara M, Rissanen A, Aromaa A, Aaran R. Serum antioxidant vitamins and risk of cataract. BMJ. 1992; 305: 1392-4. .
Jacques PF, Hartz SC, Chylack LT Jr, McGandy RB, Sadowski JA. Nutritional status in persons with and without senile cataract: blood vitamin and mineral levels. Am J Clin Nutr. 1988; 48: 152-8.
Li T, He T, Tan X, et al. Prevalence of age-related cataract in high selenium areas of China. Biol Trace Elem Res. 2009; 128: 1-7.