Scholarly article on topic 'Protective role of sesame oil against mobile base station-induced oxidative stress'

Protective role of sesame oil against mobile base station-induced oxidative stress Academic research paper on "Chemical sciences"

CC BY-NC-ND
0
0
Share paper
OECD Field of science
Keywords
{"Mobile base station" / "Oxidative stress" / "Antioxidant enzymes" / "Lipid profile" / "Testosterone hormone"}

Abstract of research paper on Chemical sciences, author of scientific article — Ebtisam A. Marzook, Ahmed E. Abd El Moneim, Abdelmonsef A. Elhadary

Abstract The present study was undertaken to shed the light on the environmental threats associated with the wireless revolution and the health hazards associated with exposure to mobile base station (MBS). Besides, studying the possible protective role of sesame oil (SO) as an antioxidant against oxidative stress. Therefore, the present work was designed to study the effect of chronic exposure to electromagnetic radiations (EMR), produced by a cellular tower for mobile phone and the possible protective role of sesame oil on glutathione reductase (GSH-Rx), superoxide dismutase (SOD), catalase (CAT), total testosterone and lipid profile (total cholesterol (Tch), triglycerides (TG), low density lipoprotein cholesterol (LDL-c) and high density lipoprotein cholesterol (HDL-c) in male albino rats. Rats were arranged into four groups: the control unexposed, the exposed untreated and the exposed treated groups (1.5 and 3 ml oil). Exposed groups were subjected to electromagnetic field at frequency of 900 MHz, for 24 h/day for 8 weeks, at the same time both treated groups were supplied with oral injection of sesame oil three times per week. At the end of the experiment, blood samples were obtained for determination of the above mentioned variables in serum. The results obtained revealed that TG and testosterone were raised significantly over control in all groups and the significant increase in oil groups occurred in dose dependent manner. SOD and CAT activities were reduced significantly in exposed rats than control and increased significantly in sesame oil groups as the dose of oil increased. Total cholesterol only showed remarkable reduction in the group treated with 3 ml sesame oil. Also, in this latter group, significant elevation of GSH-Rx was recorded. Changes in serum HDL-c and LDL-c followed an opposite trend in exposed and sesame oil groups reflecting their affectation by EMR or sesame oil. In conclusion, all results of the current study proved that sesame oil can be used as an edible oil to attenuate the oxidative stress which could be yielded as a result of chronic exposure to EMR.

Academic research paper on topic "Protective role of sesame oil against mobile base station-induced oxidative stress"

Available online at www.sciencedirect.com

ScienceDirect

Journal of Radiation Research and Applied

Sciences

journal homepage: http://www.elsevier.com/locate/jrras

Protective role of sesame oil against mobile base ^ station-induced oxidative stress

CrossMark

Ebtisam A. Marzook, Ahmed E. Abd El Moneim*, Abdelmonsef A. Elhadary

Biological Application Department, Nuclear Research Center, Atomic Energy Authority, Cairo, Egypt

ARTICLE INFO

ABSTRACT

Article history: Received 15 June 2013 Accepted 7 September 2013

Keywords:

Mobile base station Oxidative stress Antioxidant enzymes Lipid profile Testosterone hormone

The present study was undertaken to shed the light on the environmental threats associated with the wireless revolution and the health hazards associated with exposure to mobile base station (MBS). Besides, studying the possible protective role of sesame oil (SO) as an antioxidant against oxidative stress. Therefore, the present work was designed to study the effect of chronic exposure to electromagnetic radiations (EMR), produced by a cellular tower for mobile phone and the possible protective role of sesame oil on glutathione reductase (GSH-Rx), superoxide dismutase (SOD), catalase (CAT), total testosterone and lipid profile (total cholesterol (Tch), triglycerides (TG), low density li-poprotein cholesterol (LDL-c) and high density lipoprotein cholesterol (HDL-c) in male albino rats. Rats were arranged into four groups: the control unexposed, the exposed untreated and the exposed treated groups (1.5 and 3 ml oil). Exposed groups were subjected to electromagnetic field at frequency of 900 MHz, for 24 h/day for 8 weeks, at the same time both treated groups were supplied with oral injection of sesame oil three times per week. At the end of the experiment, blood samples were obtained for determination of the above mentioned variables in serum. The results obtained revealed that TG and testosterone were raised significantly over control in all groups and the significant increase in oil groups occurred in dose dependent manner. SOD and CAT activities were reduced significantly in exposed rats than control and increased significantly in sesame oil groups as the dose of oil increased. Total cholesterol only showed remarkable reduction in the group treated with 3 ml sesame oil. Also, in this latter group, significant elevation of GSH-Rx was recorded. Changes in serum HDL-c and LDL-c followed an opposite trend in exposed and sesame oil groups reflecting their affectation by EMR or sesame oil. In conclusion, all results of the current study proved that sesame oil can be used as an edible oil to attenuate the oxidative stress which could be yielded as a result of chronic exposure to EMR.

Copyright © 2013, The Egyptian Society of Radiation Sciences and Applications. Production

and hosting by Elsevier B.V. All rights reserved.

* Corresponding author.

E-mail address: drebtisam@yahoo.com (A.E. Abd El Moneim). Peer review under responsibility of The Egyptian Society of Radiation Sciences and Applications

1687-8507/$ — see front matter Copyright © 2013, The Egyptian Society of Radiation Sciences and Applications. Production and hosting by Elsevier B.V. All rights reserved. http://dx.doi.org/10.1016/jjrras.2013.10.010

1. Introduction

Recently, much attention has been directed towards the recognition of the potential health risks of radiofrequency electromagnetic waves (RF EMWs) emitted by mobile phones (Djeridane, Touitou, & de Seze, 2008). Within the past twenty years, several studies indicated a linkage between the exposure to electromagnetic radiation (EMR) and serious health problems. Electromagnetic field might produce a variety of adverse in vivo effects such as headaches, sleep disturbances, modifications of electroencephalo-graphic activity as well as alterations of biological functions in human and animals (Mossmann & Hermann, 2003; Repacholi, 2001).

Electromagnetic radiation (EMR) or radiofrequency fields of cellular phones may affect biological systems by increasing free radicals, which appear mainly to enhance lipid peroxidation and by changing the antioxidant defense systems of human tissues, thus leading to oxidative stress (Nisarg, Kavindra, & Agarwal, 2009; Ozguner et al.,

2005).

However, many studies referred another mechanism for biological disturbances; they have demonstrated that RF-EMWs from commercially available cell phones have non-thermal effects (Friedman et al., 2007; Leszczynski et al., 2002) including effects on mitochondria, apoptosis pathway, heat shock proteins, cell differentiation and DNA breaks (Leszczynski et al., 2002; McNamee et al., 2003; WHO,

2006).

RF-EMWs might disturb ROS metabolism by increasing production of ROS or by decreasing antioxidant enzyme activity. Chronic exposure to RF-EMW decreases the activity of catalase, superoxide dismutase (SOD) and glutathione perox-idase (GSH-Px), and thus reduces the total antioxidant capacity (Nisarg et al., 2009). Other study carried out by Kesari, Kumar, and Behari (2011) also demonstrated a decrease in GSH-Px and SOD with an increase in catalase. Irmak et al. (2002), on the other hand, showed that SOD activity increased in serum of rabbits exposed to EMR of digital GSM mobile telephone (900 MHz) whereas, CAT and GSH-Px were not changed (Kesari et al., 2011).

Nowadays, there is an increasing interest in discovering the protective biological function of natural compounds contained in dietary plants due to safe use, their anti-oxidative properties and their possible roles in intra and extracellular defense against oxygen radicals and lipid peroxides in response to oxidative stress. Among of these natural products, sesame oil (SO) which becomes a matter of choice for our investigation. SO was regarded in past as a daily nutritional supplement used to increase cell resistance to lipid peroxidation since it contains several antioxidants and chemo preventive agents such as tocopherol (Fukuda, 1990), sesamolin and sesaminol (Kang, Katsuzaki, & Osawa, 1998) and sesamin (Chavali, Utsunomiya, & Forse, 2001).

Hence, this investigation was undertaken to study the health hazards associated with exposure to electromagnetic waves of mobile base station for 8 weeks and to determine the

effect and the possible defense mechanisms of sesame oil on oxidative stress induced by this non-ionizing radiation.

2. Material and methods

Thirty two adult male albino rats (Rattus rattus), weighing about 150-170 g were used in this study. Animals were randomly arranged equally into four groups as follows: Control unex-posed group, EMR exposed group, EMR exposed + sesame oil-treated groups (1.5 ml and 3 ml). Electromagnetic radiation was applied to exposed groups for 8 weeks. Rats were obtained from the animal house of the Nuclear Research Center, housed in plastic cages, given standard rodents feed and tap water ad-libitum and kept under constant conditions. The treated groups were received sesame oil orally (1.5 or 3 ml) using a stomach tube three times/week according to Hsu et al. (2004).

The experimental groups were exposed to electromagnetic radiation emitted from a cellular tower (base station) for mobile phone constructed on a roof of a building in Cairo at frequency of 900 MHz, power density of 0.5 mW/cm2 at the site of exposure with distance of 8 m in front of the antenna, 24 h/day for 8 weeks. The field strength emitted by the tower was measured with isotopic probe specified for measuring high frequency and the compartment shaped to standard IEEE C 95, 1995 (N. M. El-Abiad, 2002). At the end of experiment the animals were fasting overnight, transferred to the laboratory where blood samples were collected by decapitation for laboratory assessment of the studied parameters.

Blood was allowed to clot at 37 C° for 30 min, centrifuged for 15 min at 5000 rpm, sera were separated and kept frozen at -20 °C until analysis. Serum levels oftotal testosterone, Tch, TG, LDL-c, HDL-c besides the activities of GSH-Rx, CAT and SOD were measured to evaluate the changes of the antioxidant status.

Tch and TG were estimated by using enzymatic colori-metric method of Allain et al. (1974) and Fossati and Prencipe (1982) respectively. Total testosterone hormone was assayed by using radioimmuno-assay kits supplied by Diagnostica Co., Los Angeles based on the method of Maruyama et al. (1987). Colorimetric determination of HDL-c was done using kits of Bio-Merieux Marcy-L-Etoile/France. LDL-c was calculated according to formula of Friedwald, Levy, and Fredrikeson (1972).

Serum GSH-Rx, SOD, and CAT activities were measured colorimetrically using commercial kits according to Goldberg and Spooner (1993), Nishikimi, Roa, and Yogi (1972) and Aebi (1984) respectively.

2.1. Statistical analysis

Data are expressed as means ± SE, student t-test was used to make pair wise comparison between the treatments according to Sendecor and Cochran (1989). The statistical significance was set at p < 0.05.

3. Results

Changes in serum lipid fractions in the four experimental groups are expressed in Table 1. The only significant decrease

Table 1 - Effect of sesame oil on serum lipid fractions in rats exposed to electromagnetic radiation of base station for 8 weeks.

Variables Groups

Control unexposed Group (1) Exposed Group (2) Exposed + 1.5 ml sesame oil Group (3) Exposed + 3 ml sesame oil Group(4)

Tch (mg/dl) TG (mg/dl) HDL-c (mg/dl) LDL-c (mg/dl) 48.5 ± 0.1b2 58.9 ± 0.7c1 31.2 ± 0.2a3 12.7 ± 0.1c1 48.9 ± 0.3b2 59.0 ± o.8c1 24.4 ± 0.5d1 18.5 ± 0.5a3 47.8 ± 0.3b2 67.3 ± 0.9b2 27.5 ± 0.7c2 15.7 ± 0.7b2 44.0 ± 0.6c1 90.6 ± 0.5a3 28.1 ± 1.1b2 13.8 ± 0.7c1

Data are expressed as means ± standard error for 8 rats in each group.

Values in the same row with different letters are significantly different than control group at p < 0.05. Values in the same row with different numbers are significantly different than exposed group at p < 0.05.

was noted in the group supplied with 3 ml SO as compared to the other three groups. Table 1 shows that HDL-c and LDL-c exhibited opposite trend of alteration among the experimental groups, as a function of EMR exposure and SO treatment in comparison with control group. HDL-c showed significant decrease in all exposed groups compared to control; with gradual and significant increases were seen in SO administered groups than exposed group. In contrast, the level of LDL-c expressed significant rise in exposed untreated rats and in the group treated with 1.5 ml SO as compared to control. Whereas, significant decline was noted in both oil treated groups than exposed one, although the level is still higher than control.

Contrary to Tch, the levels of TG were significantly raised in oil supplied groups than in control or exposed ones, but the increment was more evident in the group received 3 ml SO. While, no significant difference was recorded between control and exposed group.

Concerning serum total testosterone, Table 2 illustrated that the male sex hormone increased significantly in the untreated exposed group and in the groups drenched SO as compared to control group. Treatment of exposed rats with SO led to significant increment of serum total testosterone over its level in exposed untreated animals.

The data in Table 2 shows that exposure to EMR induced significant reduction in the activities of SOD and CAT without remarkable impact on GSH-Rx in comparison to control group. Treatment with SO exerted significant elevation in SOD, CAT and GSH-Rx as the dose of oil increased. But, the significant rise in GSH-Rx was only observed in rats ingested the higher dose of oil in comparison to both exposed and non-exposed control group.

4. Discussion

The widespread use of the mobile phone has initiated many studies on the possible adverse effects of a high frequency electromagnetic field (EMF), which is used in mobile phones (Hata et al., 2005).

The insignificant alteration of serum Tch levels between control animals and EMR exposed group that noted herein is in agreement with the results of N. M. El-Abiad (2002). The slight insignificant and significant reduction in the levels of serum Tch recorded in groups 3 and 4 respectively are consistent with Yokato et al. (2007). They attributed this decrement to sesamin (the major lignan constituent of SO) which have multiple functions to do in the biological system. Cholesterol-lowering and lipid-reducing actions are among its main properties via inhibiting the synthesis and absorption of cholesterol. The authors added that SO is considered a good source of vitamin E which is known as a potent antioxidant that helps in lowering cholesterol. Myung-Hwa et al. (1999) supported this concept since, they previously stated that the hypocholesterolemic action of sesamin has been referred to its ability to decrease the activity of hydroxymethylglutaryl-CoA-reductase to reduce cholesterol absorption in the intestinal tract and to increase the excretion of cholesterol into bile. Our result could also be compared with those of Yamasaki et al. (2006) who found that feeding mice on supplemental pomegranate seed oil for 3 weeks did not affect the level of serum Tch.

The data obtained herein denoted insignificant difference between control rats and EMR exposed group in the level of serum TG. This result is in accordance with the finding of N. M.

Table 2 - Effect of sesame oil on serum testosterone and variables related to oxidative stress in rats exposed to electromagnetic radiation of base station for 8 weeks.

Variables Groups

Control unexposed Group(1) Exposed Group(2) Exposed + 1.5 ml sesame oil Group(3) Exposed + 3 ml sesame oil Group(4)

Total testosterone (ng/dl) 2.2 ± 0.1d1 SOD (m/ml) 159.4 ± 1.8c1 Catalase (m/l) 672.1 ± 1.9c2 GSH-Rx (m/l) 35.5 ± 0.6b1 3.7 ± 0.1c2 77.1 ± 2.6d4 484.6 ± 1.6d1 34.0 ± 0.5b1 3.9 ± 0.1b3 134.2 ± 2.6b2 774.7 ± 2.8b3 36.3 ± 0.5b2 4.1 ± 0.1a4 270.1 ± 2.7a3 946.7 ± 3.1a4 37.7 ± 0.7a2

Means followed by the same letter (a, b or c) were not significantly different. The statistical significance was set at p < 0.05.

El-Abiad (2002) who exposed a group of female rats to microwave radiation of base station of frequency of 900-930 MHz and 0.5 mW/cm2 power density at the site of exposure, along 24 h/day for 30 days. The significant elevation of TG noted in oil ingested groups (3 and 4) over the control value in dose dependent manner. This observation could be compared with the result reported by Sankar and Rao (2006) who supplied a group of hypertensive patient with SO and instructed to use it as the only edible oil for 45 days. At the end of this period, they found no significant alterations in lipid profile of those patients as compared with their lipid profile before eating sesame oil except triglycerides. Also, our results could be compared with the finding of Yamasaki et al. (2006) who found that dietary pomegranate seed oil fed to mice for 3 weeks increases serum TG.

In the present study, serum LDL-c increased significantly in the group exposed to EMR. Meanwhile, HDL-c concomitantly declined significantly in the same group comparing to control one. These results were partially consistent with those found by N. M. El-Abiad (2002). She reported that chronic exposure to EMR was associated with a significant decrease in HDL-c and non-significant increase in LDL-c in rats.

These results could be explained on the base of EMR exposure that may be responsible for the changes of blood lipoproteins via its adverse impact on the capability of liver and intestine for synthesis of the lipid fractions contained cholesterol, or via modifying the balance between them (Mochizuki, Oda, & Yokogoshi, 1998). Moreover, peroxidation of PUFAs which occurred after exposure to EMR will modify the physiochemical properties of lipoproteins and their interaction with cell receptors (Noaman & Ibrahim, 2005; Vecera et al., 2003).

On the other hand, in groups 3 and 4 which supplemented with sesame oil, the picture of lipoprotein fractions were reversed, where the good HDL (transports cholesterol from the peripheral tissues to the liver) raised significantly and the bad LDL (transports cholesterol to peripheral tissues) declined significantly in sesame oil groups especially in group 4. These results confirmed the statement of Chaudrase Karan et al. (2007) who stated that sesame oil inhibited lipid peroxidation in rats with Acetaminophen (APAP) acute liver injury. All these results proved that sesame oil enhanced the antioxidant status and minimized lipid peroxidation.

In the current study, the significant increase in serum total testosterone in rats exposed to EMR as compared to that of control group was consistent with the same increase in the male sex hormone in rats exposed to pulsed electro - magnetic field (PEMF) about 15 and 20 pluses/day three times per week for 3 weeks with frequency of 8-12 GHz as described by Marzook (2006). The author attributed this increase to the impact of EMF on the hypothalamic centers responsible for gonadotropin releasing hormones which become less sensitive to feed back inhibition by gonadal steroid hormones. The same latter author stated that exposure to EMR may be implicated in the inhibition of melatonin secreted by the pineal gland. Several previous studies indicated that EMF exposure was related to a decrement in melatonin level and its antigonad effect (Liburdy, 1998; Stevens, 1987). Accordingly, diminished concentrations of melatonin may suppress gonadotropin secretion and hence, lead to increased release

of testosterone by the testis. The significant elevation in serum testosterone levels in the groups of rats fed standard rodent diet enriched with SO as recorded herein came in parallel with he results of El-Shafey, Ali, and Marzook (2009) who found significant increase in serum testosterone in male rats exposed to EMF-900 MHz emitted from mobile station antenna for 4 weeks simultaneously with nourishment on a diet supplemented with garlic oil. They attributed this significant increase over the exposed group to the possible rise in the level of sex hormones binding globulin induced by garlic oil which is rich in its content of antioxidants as well as SO. Accordingly, the testis was forced to secrete more testosterone in the blood stream. Another alternative interpretation was suggested by the same authors based on the stimulation of the pituitary gonadal axis induced by garlic oil to release more LH which stimulated the testis to increase its testosterone production.

The remarkable reduction in the activities of SOD, CAT and GSH-Rx concomitantly occurred in rats exposed to EMR (group 2) indicated that those animals suffered from oxidative stress. Ahmadpoor et al. (2009) stated that oxidative stress occurred as a consequence of imbalance between reactive oxygen species (ROS) and body antioxidant capacity. Thus, this Phenomenon could be happened as a result of increased ROS generation, impaired antioxidant defense system or a combination of both. SOD, CAT and GSH-Rx are enzymes naturally developed by the mammalian body as endogenous antioxi-dant system to deal with reactive oxygen intermediates. SOD dismutases the superoxide anion radicals to H2O2 and H2O (Lawler & Song, 2002). CAT catalyses the decomposition of H2O2 to H2O and oxygen (Spolaries & Wu, 1997). Glutathione is a well-known antioxidant and GSH-Rx metabolizes H2O2 to H2O. In this process, glutathione gets oxidized and forms oxidized glutathione. The oxidized glutathione is reduced back to glutathione in the presence of the enzyme called glutathione reductase (Bayse, Baker, & Ortwine, 2005; Russel, 1998).

However, it becomes more effective when the oxidative stress is extreme, ROS scavenging enzyme such as SOD and CAT are degraded as noted in the exposed group in this Study.

In the current study, when EMR exposed animals were supplied with SO, the above mentioned enzymes tended to rise in the sera of group 3 and 4 in a dose dependent manner to be superior than that of control in order to face and overcome the oxidative stress. These results came in accordance with the findings of Snakar and Rao (2006) who found obvious increase in the activities of SOD and CAT accompanied with a decrease in lipid peroxidation as identified by an adduction of thiobarbituric acid reactive substances (TBARS) after 45 days of supplying a group of hypertensive patients with SO as the only edible oil to be eaten in that period. All these findings indicate that SO is a potent antioxidant rich oil as it possesses some preventive substances such as sesamin, sesaminol and sesamolin besides its wealth with fat soluble vitamins like tocopherol (Fukuda, 1990). In general our results confirmed what has been reported by Chaudrase Karan et al. (2007). They stated that sesame oil maintained the intracellular glutathione levels and reduced ROS levels in rats with acetaminophen (APAP) induced acute liver injury.

5. Conclusion

From these results we may conclude that sesame oil can be used as an antioxidant to attenuate the oxidative stress which could be yielded as a result of chronic exposure to EMR by increasing antioxidant enzymes activity.

REFERENCES

Aebi, H. (1984). Catalase. In H. U. Bergmeyer (Ed.), Methods Enzymol.Methods of enzymatic analysis (pp. 105121-105126).

Ahmadpoor, P., Eftekhar, E., Nourooz-Zadeh, J., Servat, H.,

Makhdoomi, K., & Ghafari, A. (2009). Glutathione, glutathione-related enzymes, and total antioxidant capacity in patients on maintenance dialysis. Iranian Journal of Kidney Diseases, 3(1), 22-27.

Allain, C. C., Poon, L. S., Chain, C. S. G., Richmond, W., & Fu, C. (1974). Enzymatic determinations of total serum cholesterol. Clinical Chemistry, 20(4), 470-475.

Bayse, C. A., Baker, R. A., & Ortwine, K. N. (2005). Relative strength of selenium. Implications for glutathione peroxidase activity. Inorganic Chimica Acta, 358(1), 3849-3854.

Chaudrase Karan, V. R., Wan, C. H., Liu, L. L., Hus, D. Z., & Liu, M. (2007 Dec.). Effect of sesame oil against acetaminophen induced acute oxidative hepatic damage in rats. Shock, 13.

Chavali, S. R., Utsunomiya, T., & Forse, R. A. (2001). Increased survival after cecal ligation and puncture in mice consuming diets enriched with sesame oil. Critical Care Medicine, 29,140-143.

Djeridane, Y., Touitou, Y., & de Seze, R. (2008). Influence of EMF by GSM-900 cellular telephones on the circadian patterns of gonadal adrenal and pituitary hormones in men. Radiation Research, 169(3), 337-343.

El-Abiad, N. M. (2002). Influence of pineal hormone on serum estradiol, catecholamines and lipid fractions in female rats exposed to electromagnetic radiation of base station for cellular telephone. Egyptian Journal of Applied Sciences, 17(7), 405-419.

El-Shafey, A. A., Ali, E. A., & Marzook, E. A. (2009). Effect of garlic oil on hematological parameters, blood respiration functions and serum testosterone in male rats exposed to electromagnetic field. Isotope Radiation Research, 41(2), 397-410.

Fossati, P., & Prencipe, L. (1982). Serum triglycerides determined with an enzyme that produces hydrogen peroxide. Clinical Chemistry, 28, 2077-2080.

Friedman, J., Kraus, S., Hauptman, Y., Schiff, Y., & Seger, R. (2007). Mechanism of short-term ERK activation by electromagnetic fields at mobile phone frequencies. Biochemical Journal, 405, 559-568.

Friedwald, W. T., Levy, R. I., & Fredrikeson, D. S. (1972). Estimation of the concentration of low density lipoprotein cholesterol in plasma without use of preparative ultracentrifuge. Clinical Chemistry, 18, 499-502.

Fukuda, Y. (1990). Food chemical studies on the antioxidants in sesame seed. Nippon Shokuhin Kogyo Gakkaishi, 37, 484-492.

Goldberg, D. M., & Spooner, R. J. (1993). In (3rd ed.). Methods of enzymatic analysis (Vol. 3; pp. 258-265) Deerfield beach, FI: Verlog Chemie.

Hata, K., Yamaguchi, H., Tsurita, G., Watanabe, S., Wake, K., Taki, M., et al. (2005). Short term exposure to 1439 MHz pulsed TDMA field does not alter melatonin synthesis in rats. Bioelectromagnetics, 26(1), 49-53.

Hsu, D. Z., Chiang, P. J., Chein, S. P., Huang, B. M., & Liu, M. Y. (2004). Parenteral sesame oil attenuates oxidative stress after endotoxin in toxication in rats. Toxicology, 196, 147-153.

Irmak, M. K., Fadillioglu, E., Gulec, M., Erdogan, H., Yagmurca, M., & Akyol, O. (2002). Effects of electromagnetic radiation from a cellular telephone on the oxidant and antioxidant levels in rabbits. Cell Biochemistry and Function, 20(4), 279-283.

Kang, M. H., Katsuzaki, H., & Osawa, T. (1998). Inhibition of 2,2'-azobist (2,4-dimethyl-valeronitrile)-induced lipid peroxidation by sesaminols. Lipid, 33, 1031-1036.

Kesari, K. K., Kumar, S., & Behari, J. (2011). Effects of

radiofrequency electromagnetic wave exposure from cellular phones on the reproductive pattern in male Wistar rats. Applied Biochemistry and Biotechnology, 15.

Lawler, I. M., & Song, W. (2002). Specificity of antioxidant enzyme inhibition in skeletal muscle to reactive nitrogen species donors. Biochemical and Biophysical Research Communications, 294, 1093-1100.

Leszczynski, D., Joenvaara, S., Reivinen, J., & Kuokka, R. (2002). Non-thermal activation of the hsp27/p38MAPK stress pathway by mobile phone radiation in human endothelial cells: molecular mechanism for cancer- and blood-brain barrier-related effects. Differentiation, 70, 120-129.

Liburdy, R. (1998). Role of mechanistic data in strengthening the epidemiology findings (pp. 12-14). EMF RAPID, Breakout Group Reports for Epidemiological Research Findings, San Antonio, Texas.

Maruyama, Y., Aoki, N., Suzuki, Y., Ohno, Y., & Imamura, M. (1987). Sex-steroid-binding plasma protein (SBP), testosterone, estradiol and DHEA in prepuberty and puberty. Acta Endocrinologica, 114(1), 60-67.

Marzook, E. A. (2006). Effect of pulsed electromagnetic field on some biochemical and hematological parameters of female rats. Isotope Radiation Research, 38(4 Suppl.), 1245-1256.

McNamee, J. P., Bellier, P. V., Gajda, G. B., Lavallee, B. F., Marro, L., & Thansandote, A. (2003). No evidence for genotoxic effects from 24 h exposure of human leukocytes to 1.9 GHz radiofrequency fields. Radiation Research, 159, 693-697.

Mochizuki, H., Oda, H., & Yokogoshi, H. (1998). Increasing effect of dietary taurine on serum HDL cholesterol concentration in rats. Bioscience, Biotechnology, and Biochemistry, 62, 578-579.

Mossmann, K. A., & Hermann, D. M. (2003). Effects of

electromagnetic radiations of mobile phones on the central nervous system. Bioelectromagnetics, 24(1), 49-62.

Myung -Hwa, K., Yoshichika, K., Michitaka, N., & Toshihiko, O. (1999). Dietary defatted sesame flour decreases susceptibility to oxidative stress in hypercholesterolemic rabbits. Journal of Nutrition, 129, 1885-1890.

Nisarg, R. D., Kavindra, K. K., & Agarwal, A. (2009).

Pathophysiology of cell phone radiation: oxidative stress and carcinogenesis with focus on male reproductive system. Reproductive Biology and Endocrinology, 7, 114.

Nishikimi, M., Roa, N. A., & Yogi, k. (1972). The occurrence of superoxide anion in the reaction of reduced phenazine methosulfate and molecular oxygen. Biochemical and Biophysical Research Communications, 46, 849-854.

Noaman, S. M., & Ibrahim, N. (2005). Egyptian Journal of Radiation Science Applications, 18(2), 259.

Ozguner, F., Altinbas, A., Ozaydin, M., Dogan, A., Vural, H., Kisioglu, A. N., & Cesur, G. (2005). Mobile phone-induced myocardial oxidative stress: protection by a novel antioxidant agent caffeic acid phenethyl ester. Toxicology and Industrial Health, 21(9), 223-230.

Repacholi, M. H. (2001). Health risks from the use of mobile phones. Toxicology Letters, 120(1-3), 323-331.

Russel, J. R. (1998). Oxidative damage in the central nervous system. Protection by melatonin. Progress in Neurobiology, 56, 359-384.

Sankar, D., & Rao, M. R. (2006). Effect of sesame oil on diuretics or beta-blockers in the modulation of blood pressure, anthropometry, lipid profile and redox status. Yale Journal of Biology and Medicine, 79(1), 10-26.

Sendecor, G. W., & Cochran, W. G. (1989). Statistical methods (8th ed.). Ames, Iowa, USA: Saint Louis State Univ. Press.

Spolaries, Z., & Wu, J. X. (1977). Role of glutathione and catalase in H2O2 detoxification in LSP-activated hepatic endothelial and Kupffer cells. American Journal of Physiology, 36, G1304—G1311.

Stevens, R. G. (1987). Electric power use and breast cancer: a hypothesis. American Journal of Epidemiology, 125, 556—561.

Vecera, R., Skottova, N., Vana, P., Kazdova, L., Chmela, Z.,

Svagera, Z., et al. (2003). Antioxidant status, lipoprotein profile and liver lipids in rats fed on high cholesterol diet containing currant oil rich in 2-3 and n-6 polyunsaturated fatty acids. Physiological Research, 52, 177—187.

World Health Organization. (2006). WHO research agenda for radio frequency fields. www.who.int/peh-emf/research/agenda/en/ index 2.html.

Yamasaki, M., Kitagawa, T., Koyanagi, N., Chujo, H., Maeda, H., Kohno-Murase, J., et al. (2006 Jan.). Dietary effect of pomegranate seed oil on immune function and lipid metabolism in mice. Nutrition, 22(1), 54-59.

Yokora, T., Matsuzaki, Y., Koya, M., Hitomi, T.,

Kawanaka, M., Enoki-Konishi, M., et al. (2007 Sep). Sesamin, a lignan of sesame, down-regulates cyclin D1 protein expression in human tumor cells. Cancer Science, 98(9), 1447-1453.