Molecular Vision: Effects of computer monitor-emitted radiation on oxidant/antioxidant balance in cornea and lens from rats

Molecular Vision 2009; 15:2521-2525 <>
Received 9 July 2009 | Accepted 26 November 2009 | Published 2 December 2009

Effects of computer monitor-emitted radiation on oxidant/antioxidant balance in cornea and lens from rats

Mehmet Balci,1 Mehmet Namuslu,2 Erdinç Devrim,2 İlker Durak2

1Dr. Abdurrahman Yurtaslan Oncology Training and Research Hospital, Department of Ophthalmology, Ankara, Turkey; 2Ankara University, Faculty of Medicine, Department of Biochemistry, Ankara, Turkey

Correspondence to: Mehmet Balci, Ceyhun Atuf Kansu Caddesi 16. Sokak No. 6/7, 06520 Balgat/Ankara, Turkey; Phone: +90 312 473 46 45; email:


Purpose: This study aims to investigate the possible effects of computer monitor-emitted radiation on the oxidant/antioxidant balance in corneal and lens tissues and to observe any protective effects of vitamin C (vit C).

Methods: Four groups (PC monitor, PC monitor plus vitamin C, vitamin C, and control) each consisting of ten Wistar rats were studied. The study lasted for three weeks. Vitamin C was administered in oral doses of 250 mg/kg/day. The computer and computer plus vitamin C groups were exposed to computer monitors while the other groups were not. Malondialdehyde (MDA) levels and superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) activities were measured in corneal and lens tissues of the rats.

Results: In corneal tissue, MDA levels and CAT activity were found to increase in the computer group compared with the control group. In the computer plus vitamin C group, MDA level, SOD, and GSH-Px activities were higher and CAT activity lower than those in the computer and control groups. Regarding lens tissue, in the computer group, MDA levels and GSH-Px activity were found to increase, as compared to the control and computer plus vitamin C groups, and SOD activity was higher than that of the control group. In the computer plus vitamin C group, SOD activity was found to be higher and CAT activity to be lower than those in the control group.

Conclusion: The results of this study suggest that computer-monitor radiation leads to oxidative stress in the corneal and lens tissues, and that vitamin C may prevent oxidative effects in the lens.


An increasing number of people report subjective symptoms and hypersensitivity to a wide variety of electromagnetic sources including power lines, radio and TV broadcasting stations, cellular phones, and computer monitors [1]. A personal computer (PC) is standard equipment for many people in industrialized societies, and its use is growing. A PC user is exposed to an electromagnetic field (EMF), visible and ultraviolet light, radio-range waves, and extremely low frequency (50 Hz) fields (ELF) [2]. Preliminary experiments showed that radiation from a monitor can produce potentially hazardous biological effects [2].

There is increasing interest in the potential health risks and biologic effects related to exposure to ELF-EMFs. Among the environmental risk factors that affect human health, ELF-EMFs play an important role because of their possible association with childhood malignancy, especially leukemia, but also cancer and cardiovascular, neurological, and psychological diseases in adults [3-6]. The incidence of premature births and infants born with pathologies and the risk of brain tumors are higher for PC users [7]. PC monitor radiation stimulates the growth of urethane-induced lung tumors in mice [8]. Although eye-related effects of PC monitor use have not yet been discovered, past studies have demonstrated a relation between electromagnetic radiation (EMR) and cataracts [9]. Corneal and retinal damage has been observed as well [10,11].

Much research interest has emerged about the mechanisms of the interaction between ELF-EMFs and living organisms. Experimental studies have shown that ELF-EMFs may interfere with chemical reactions involving free radical production [12-14]. Moreover, some researchers have reported that PC monitor use is associated with the free radical process [2,15]. The eye is an exceptional organ because of its continuous exposure to environmental chemicals, radiation, and atmospheric oxygen. Oxidative stress mechanisms in ocular tissues have been hypothesized to play a role in diseases such as cataracts, glaucoma, uveitis, pseudoexfoliation syndrome, and age-related macular degeneration [16,17].

Vitamin C (vit C), a powerful antioxidant, provides a protective effect against several diseases, including oxidative imbalances arising from various causes in the lens [18-20]. At the same time, vit C acts as a pro-oxidant, depending upon the environment in which the molecule is present. It has been reported that millimolar concentrations of vit C induced apoptotic cell death, characterized by cell shrinkage, nuclear fragmentation, and internucleosomal DNA cleavage in human myelogenous leukemic cell lines. Higher concentrations of vit C induce apoptotic cell death in various tumor cell lines, including oral squamous cell carcinoma and salivary gland tumor cell lines, possibly via its pro-oxidant action. The apoptosis-inducing activity of vit C is stimulated by Cu2+, lignin, and ion chelator and inhibited by catalase, Fe3+, and Co2+. As far as we know, there is no study in the existing literature investigating the possible protective effects of vit C against PC monitor radiation in the corneal and lens tissues [20-25].

The aim of the present study is to investigate the effects of PC monitor-emitted radiation on oxidative stress and antioxidant enzyme activities in the corneal and lens tissues of rats and to observe any protective effects of vitamin C.


Forty female Wistar albino type rats (average 160 g and six weeks old, in puberty period) were used in the study. The study was approved by the Ethics Committee of Ankara Oncology Hospital. The animals received appropriate animal care, and the study protocol complied with the institution’s guidelines of the Health Ministry. Four groups were constituted, and in each group (control, PC monitor, PC monitor plus vitamin C, and vitamin C) there were ten animals. The PC monitor group was exposed to two cathode ray tube (CRT) type monitors positioned face-to-face, approximately 20 cm away from the cages. Brightness/contrast settings were adjusted to 50% of the maximum levels of each.

The PC monitor plus vitamin C group was exposed to the same monitors and received vitamin C in solution form, in oral doses of 250 mg kg−1 day−1 [26]. The vitamin C group was treated with vitamin C only, in the same manner. The PC monitor groups were exposed to an EMF for 8 h/day, every day, for a period of three weeks. The rats were group-caged and were allowed free motion in their cages. The control and vitamin C groups were in another room in which there was no EMF. Throughout the study period, these two groups were never exposed to an EMF.

During the study, all the animals, including the control group, were fed a laboratory diet and water ad libitum. At the end of the study period, the animals were sacrificed under ether anesthesia and their corneal and lens tissues were surgically dissected. The tissues were homogenized and prepared for the assays as described previously [27]. The upper, clear part of the tissue homogenates (supernatants) was used in the measurements. The protein levels of the clear supernatants were studied using the Lowry method [28]. MDA levels (nmol/mg), SOD (U/mg), GSH-Px (mIU/mg), and CAT (IU/mg) enzyme activities were measured from the supernatants. MDA levels were measured by the thiobarbituric acid reactive substances (TBARS) method [29]. SOD activity was measured as described previously [30]. One unit for SOD activity was expressed as the enzyme protein amount causing 50% inhibition in the nitro blue tetrazolium (NBT) reduction rate. Catalase activity was determined by measuring the absorbance decrease of H2O2 at 240 nm [31]. GSH-Px activity was measured by following changes in nicotinamide adenine dinucleotide phosphate (NADPH) absorbance at 340 nm [32]. In the activity calculations, extinction coefficients of H2O2 (40.98 L mol-1 cm-1 at 240 nm) and NADPH (6220 L mol-1 cm-1 at 340 nm) were used for CAT and GSH-Px enzymes, respectively.

All statistical analyses were carried out using SPSS statistical software (SPSS for Windows, version 12.0, SPSS Inc., Chicago, IL). Data were given as arithmetic mean ±standard deviation (mean±SD). In the statistical evaluation of the results, the Student’s t test was carried out. Statistical significance was defined as a p value lower than 0.05.


The corneal and lens levels of the oxidative parameters for all groups are given in Table 1 and Table 2, respectively. In the corneal tissue, there were significant increases in the MDA level and CAT activity in the PC monitor group, compared with the control group (p<0.05), whereas there was no difference in SOD and GSH-Px activities between the two groups. In the PC monitor plus vitamin C group, the MDA level, SOD, and GSH-Px activities were significantly higher, and CAT activity was significantly lower, compared with the corresponding values in the PC monitor group (p<0.05). In the PC monitor plus vitamin C group, the MDA level, SOD, and GSH-Px activities were significantly higher (p<0.05), and CAT activity was significantly lower (p<0.05) than in the control group.

In the results obtained for lens tissue, the MDA level, SOD, and GSH-Px activities were confirmed to be significantly increased in the PC monitor group relative to the control group (p<0.05). As for CAT activity, no significant difference was found between the two groups. When the PC monitor group was compared with the PC monitor plus vitamin C group, significantly lower MDA levels and GSH-Px activity were found in the latter group (p<0.05). No significant differences were seen between the two groups in terms of SOD and CAT activities. In the PC monitor plus vitamin C group, SOD activity was significantly higher (p<0.05), and CAT activity was significantly lower (p<0.05) than in the control group.


In order to explain the epidemiological observations associated with ELF-EMF exposure, experiments have been conducted in multiple laboratories to examine alterations of biological functions by EMF at the cellular and molecular levels. Cellular studies have described a variety of EMF effects on biological and biochemical responses, including cell proliferation [33,34], cell surface properties [35], apoptosis induction [36], and DNA damage [37]. Among the putative mechanisms, ELF-EMFs may affect biological systems by increasing free radical life span and the concentration of free radicals (or other reactive oxygen species - ROS) in cells [12,38-41].

It is well known that ROS lead to oxidative damage in major cell macromolecules, such as lipids and nucleic acids. ROS have been implicated in tissue injury. The main ROS that have to be considered are the superoxide anion (O2-.), which is predominantly generated by the mitochondria; H2O2 produced from O2-. by the action of SOD; and peroxynitrite generated by the reaction of O2-. with nitric oxide. ROS are scavenged by SOD, GSH-Px, and CAT. MDA is the breakdown product of the major chain reactions leading to the oxidation of polyunsaturated fatty acids and, thus, serves as a reliable marker of oxidative stress-mediated lipid peroxidation [42].

The disruption of the oxidant/antioxidant balance in the eye and other tissues exposed to EMR from mobile phones has been shown in experimental studies [11,43]. In addition, we found that mobile phone radiation leads to oxidative stress due to increased MDA levels in the cornea and lens [44]. Falone et al. [45] indicated that ELF-EMF exposure significantly affects anti-oxidative capability, and they suggested that exposure to ELF-EMFs may act as a risk factor for the occurrence of oxidative stress-based nervous system pathologies. Moreover, some researchers have recently linked the role of ELF-EMFs in activating immune-relevant cell types to the free radical-based physiological changes detected following field exposure [46,47].

Yokus et al. [38] reported increased lipid peroxidation oxidative DNA damage in rats exposed to ELF-EMFs. Furthermore, Guler et al. [48] found a significant increase in the levels of MDA and a significant decrease in antioxidant enzyme activities in Guinea pigs that were exposed to an ELF-electric field. They also indicated that N-acetyl-L-cysteine application has protective effects on ELF-electric field-induced oxidative stress. In the present study, we detected clear changes due to oxidative stress in the cornea, in accordance with previous studies. In corneas exposed to PC monitor radiation, the MDA level, as an indicator of lipid peroxidation, significantly increased. The cornea, being lipid-rich tissue, may manifest this marked increase in MDA [49].

A number of studies have been performed to evaluate the antioxidant effects on EMF-induced oxidative damage [11,43]. We also investigated the effectiveness of a powerful antioxidant, vitamin C, on the oxidative damage induced by monitor radiation under the present experimental conditions. Vitamin C treatment on the radiation-exposed groups resulted in significantly increased SOD and GSH-Px activities. However, vitamin C could not protect corneal tissue against PC monitor radiation-induced oxidative stress, as revealed by increased MDA levels, and decreased catalase activity, in the PC monitor plus vitamin C group compared to the PC monitor group.

In the lens tissue, significantly increased MDA levels, SOD, and GSH-Px activities were found in the group exposed to radiation compared to the control group. SOD and GSH-Px activities may increase as a compensatory mechanism to eliminate this oxidative stress. We observed a significant decrease in MDA levels in the lens tissue with the administration of vitamin C in the PC monitor group, compared to the PC monitor alone group. Additionally, SOD activity was higher in the PC monitor plus vitamin C group than in the control group.

In conclusion, exposure to PC monitor radiation may act as a risk factor for the occurrence of oxidative stress-based cornea and lens pathologies. The potent free radical scavenger and antioxidant, vitamin C, may protect lens tissues from oxidative damage, thus preventing organ dysfunction. Considering the widespread use of computers, it will be essential to evaluate the long-term effects of computer monitor radiation on the eye, as well as protective measures. There is a need for further study with different frequencies and exposure periods in order to discover the effects of PC monitor radiation-induced oxidative stress in the eye.


  1. Mortazavi SM, Ahmadi J, Shariati M. Prevalence of subjective poor health symptoms associated with exposure to electromagnetic fields among university students. Bioelectromagnetics. 2007; 28:326-30. [PMID: 17330851]
  2. Anisimov VN, Arutiunian AV, Burmistrov SO, Zabezhinskiĭ MA, Muratov EI, Oparina TI, Popovich IG, Prokopenko VM, Frolova EV. Effects of radiation from video display terminals of personal computers on free radical processes in rats. Biull Eksp Biol Med. 1997; 124:192-4. [PMID: 9410208]
  3. Davanipour Z, Tseng CC, Lee PJ, Sobel E. A case-control study of occupational magnetic field exposure and Alzheimer's disease: results from the California Alzheimer's Disease Diagnosis and Treatment Centers. BMC Neurol. 2007; 7:13 [PMID: 17559686]
  4. Hakansson N, Gustavsson P, Sastre A, Floderus B. Occupational exposure to extremely low frequency magnetic fields and mortality from cardiovascular disease. Am J Epidemiol. 2003; 158:534-42. [PMID: 12965879]
  5. Loomis DP, Savitz DA. Mortality from brain cancer and leukaemia among electrical workers. Br J Ind Med. 1990; 47:633-8. [PMID: 2207035]
  6. Wertheimer N, Leeper E. Electrical wiring configurations and childhood cancer. Am J Epidemiol. 1979; 109:273-84. [PMID: 453167]
  7. Pinholster G. The Cheshire cat phenomenon: effects of nonionizing electromagnetic radiation. Environ Health Perspect. 1993; 101:292-5. [PMID: 8275983]
  8. Anisimov VN, Popovich IG, Zabezhinskii MA, Muratov EI, Nikitina VN, Kalinina NI. Effect of radiation emitted from personal computer terminal on urethan-induced lung tumors in mice. Vopr Onkol. 1996; 42:77-81. [PMID: 8686250]
  9. Stewart-DeHaan PJ, Creighton MO, Larsen LE, Jacobi JH, Ross WM, Sanwal M, Guo TC, Guo WW, Trevithick JR. In vitro studies of microwave-induced cataract: separation of field and heating effects. Exp Eye Res. 1983; 36:75-90. [PMID: 6825735]
  10. Kues HA, Hirst LW, Lutty GA, D'Anna SA, Dunkelberger GR. Effects of 2.45-GHz microwaves on primate corneal endothelium. Bioelectromagnetics. 1985; 6:177-88. [PMID: 4004950]
  11. Ozguner F, Bardak Y, Comlekci S. Protective effects of melatonin and caffeic acid phenethyl ester against retinal oxidative stress in long-term use of mobile phone: a comparative study. Mol Cell Biochem. 2006; 282:83-8. [PMID: 16317515]
  12. Brocklehurst B, McLauchlan KA. Free radical mechanism for the effects of environmental electromagnetic fields on biological systems. Int J Radiat Biol. 1996; 69:3-24. [PMID: 8601753]
  13. Simko M. Cell type specific redox status is responsible for diverse electromagnetic field effects. Curr Med Chem. 2007; 14:1141-52. [PMID: 17456027]
  14. Simko M, Mattsson MO. Extremely low frequency electromagnetic fields as effectors of cellular responses in vitro: possible immune cell activation. J Cell Biochem. 2004; 93:83-92. [PMID: 15352165]
  15. Anisimov VN, Zabezhinskii MA, Muratov EI, Popovich IG, Arutiunian AV, Oparina TI, Prokopenko VM. Effect of irradiation from a personal computer video terminal on estrus function, melatonin level, and free radical processes in laboratory rodents. Biofizika. 1998; 43:165-70. [PMID: 9567194]
  16. Ohia SE, Opere CA, Leday AM. Pharmacological consequences of oxidative stress in ocular tissues. Mutat Res. 2005; 579:22-36. [PMID: 16055157]
  17. Yagci R, Ersoz I, Erdurmus M, Gurel A, Duman S. Protein carbonyl levels in the aqueous humour and serum of patients with pseudoexfoliation syndrome. Eye. 2008; 22:128-31. [PMID: 17293783]
  18. Mayer UM, Muller Y, Bluthner K. Vitamins C and E protect cultures of bovine lens epithelium from the damaging effects of blue light (430 nm) and UVA light (300-400 nm). Klin Monatsbl Augenheilkd. 2001; 218:116-20. [PMID: 11258123]
  19. Hegde KR, Varma SD. Protective effect of ascorbate against oxidative stress in the mouse lens. Biochim Biophys Acta. 2004; 1670:12-8. [PMID: 14729137]
  20. Simsek M, Naziroglu M, Erdinc A. Moderate exercise with a dietary vitamin C and E combination protects against streptozotocininduced oxidative damage to the kidney and lens in pregnant rats. Exp Clin Endocrinol Diabetes. 2005; 113:53-9. [PMID: 15662597]
  21. Chen Q, Espey MG, Sun AY, Pooput C, Kirk KL, Krishna MC, Khosh DB, Drisko J, Levine M. Pharmacologic doses of ascorbate act as a prooxidant and decrease growth of aggressive tumor xenografts in mice. Proc Natl Acad Sci USA. 2008; 105:11105-9. [PMID: 18678913]
  22. Chen Q, Espey MG, Sun AY, Lee J-H, Krishna MC, Shacter E, Choyke PL, Pooput C, Kirk KL, Buettner GR, Levine M. Ascorbate in pharmacologic concentrations selectivelygenerates ascorbate radical and hydrogen peroxide in extracellular fluid in vivo. Proc Natl Acad Sci USA. 2007; 104:8749-54. [PMID: 17502596]
  23. Nelli S, Craig J, Martin W. Oxidation by trace Cu2+ ions underlies the ability of ascorbate to induce vascular dysfunction in the rat perfused mesentery. Eur J Pharmacol. 2009; 614:84-90. [PMID: 19394330]
  24. Stadtman ER. Ascorbic acid and oxidative inactivation of proteins. Am J Clin Nutr. 1991; 54:1125S-8S. [PMID: 1962558]
  25. Wróblewski K. Can the administration of large doses of vitamin C have a harmful effect? Pol Merkur Lekarski. 2005; 19:600-3. [PMID: 16379336]
  26. Ueta E, Tadokoro Y, Yamamoto T, Yamane C, Suzuki E, Nanba E, Otsuka Y, Kurata T. The effect of cigarette smoke exposure and ascorbic acid intake on gene expression of antioxidant enzymes and other related enzymes in the livers and lungs of Shionogi rats with osteogenic disorders. Toxicol Sci. 2003; 73:339-47. [PMID: 12700399]
  27. Kavutcu M, Canbolat O, Ozturk S, Olcay E, Ulutepe S, Ekinci C, Gökhun IH, Durak I. Reduced enzymatic antioxidant defense mechanism in kidney tissues from gentamicin-treated guinea pigs: effects of vitamins E and C. Nephron. 1996; 72:269-74. [PMID: 8684538]
  28. Lowry OH, Rosebrough NJ, Farr AL, Randall RJ. Protein measurement with the Folin phenol reagent. J Biol Chem. 1951; 193:265-75. [PMID: 14907713]
  29. Dahle LK, Hill EG, Holman RT. The thiobarbituric acid reaction and the autoxidations of polyunsaturated fatty acid methyl esters. Arch Biochem Biophys. 1962; 98:253-61. [PMID: 13883105]
  30. Durak I, Canbolat O, Kavutcu M, Ozturk HS, Yurtarslani Z. Activities of total, cytoplasmic, and mitochondrial superoxide dismutase enzymes in sera and pleural fluids from patients with lung cancer. J Clin Lab Anal. 1996; 10:17-20. [PMID: 8926562]
  31. Aebi H. Catalase. Catalase, New York: Academic Press Inc; 1974. p. 673-7.
  32. Paglia DE, Valentine WN. Studies on the quantitative and qualitative characterization of erythrocyte glutathione peroxidase. J Lab Clin Med. 1967; 70:158-69. [PMID: 6066618]
  33. Blackman CF, Blanchard JP, Benane SG, House DE, Elder JA. Double blind test of magnetic field effects on neurite outgrowth. Bioelectromagnetics. 1998; 19:204-9. [PMID: 9581963]
  34. Pirozzoli MC, Marino C, Lovisolo GA, Laconi C, Mosiello L, Negroni A. Effects of 50 Hz electromagnetic field exposure on apoptosis and differentiation in a neuroblastoma cell line. Bioelectromagnetics. 2003; 24:510-6. [PMID: 12955756]
  35. Paradisi S, Donelli G, Santini MT, Straface E, Malorni W. A 50-Hz magnetic field induces structural and biophysical changes in membranes. Bioelectromagnetics. 1993; 14:247-55. [PMID: 8391817]
  36. Hisamitsu T, Narita K, Kasahara T, Seto A, Yu Y, Asano K. Induction of apoptosis in human leukemic cells by magnetic fields. Jpn J Physiol. 1997; 47:307-10. [PMID: 9271162]
  37. Yokus B, Cakir DU, Akdag MZ, Sert C, Mete N. Oxidative DNA damage in rats exposed to extremely low frequency electro magnetic fields. Free Radic Res. 2005; 39:317-23. [PMID: 15788236]
  38. Lai H, Singh NP. Acute exposure to a 60 Hz magnetic field increases DNA strand breaks in rat brain cells. Bioelectromagnetics. 1997; 18:156-65. [PMID: 9084866]
  39. Singh N, Lai H. 60 Hz magnetic field exposure induces DNA crosslinks in rat brain cells. Mutat Res. 1998; 400:313-20. [PMID: 9685689]
  40. Grissom CB. Magnetic field effects in biology: A survey of possible mechanisms with emphasis on radical-pair recombination. Chem Rev. 1995; 95:3-24.
  41. Lee BC, Johng HM, Lim JK, Jeong JH, Baik KY, Nam TJ, Lee JH, Kim J, Sohn UD, Yoon G, Shin S, Soh KS. Effects of extremely low frequency magnetic field on the antioxidant defense system in mouse brain: a chemiluminescence study. J Photochem Photobiol B. 2004; 73:43-8. [PMID: 14732250]
  42. de Zwart LL, Meerman JHN, Commandeur JNM, Vermeulen NPE. Biomarkers of free radical damage:applications in experimental animals and in humans. Free Radic Biol Med. 1999; 26:202-26. [PMID: 9890655]
  43. Ilhan A, Gurel A, Armutcu F, Kamisli S, Iraz M, Akyol O, Ozen S. Ginkgo biloba prevents mobile phone-induced oxidative stress in rat brain. Clin Chim Acta. 2004; 340:153-62. [PMID: 14734207]
  44. Balci M, Devrim E, Durak I. Effects of mobile phones on oxidant/antioxidant balance in cornea and lens of rats. Curr Eye Res. 2007; 32:21-5. [PMID: 17364731]
  45. Falone S, Mirabilio A, Carbone MC, Zimmitti V, Di Loreto S, Mariggiò MA, Mancinelli R, Di Ilio C, Amicarelli F. Chronic exposure to 50Hz magnetic fields causes a significant weakening of antioxidant defense systems in aged rat brain. Int J Biochem Cell Biol. 2008; 40:2762-70. [PMID: 18585472]
  46. Frahm J, Lantow M, Lupke M, Weiss DG, Simko M. Alteration in cellular functions in mouse macrophages after exposure to 50 Hz magnetic fields. J Cell Biochem. 2006; 99:168-77. [PMID: 16598759]
  47. Lupke M, Frahm J, Lantow M, Maercker C, Remondini D, Bersani F, Simkó M.. Gene expression analysis of ELF-MF exposed human monocytes indicating the involvement of the alternative activation pathway. Biochim Biophys Acta. 2006; 1763:402-12. [PMID: 16713449]
  48. Guler G, Turkozer Z, Tomruk A, Seyhan N. The protective effects of N-acetyl-L-cysteine and epigallocatechin-3-gallate on electric field-induced hepatic oxidative stress. Int J Radiat Biol. 2008; 84:669-80. [PMID: 18661381]
  49. Bazan HEP. Cellular and molecular events in corneal wound healing: significance of lipid signalling. Exp Eye Res. 2005; 80:453-63. [PMID: 15781273]