The antioxidative effect of far-infrared radiation (FIR) in human was evaluated by half maximal inhibitory concentration of blood against superoxide anions. All samples ranging from 18 to 30 years old were grouped into sympathetic, parasympathetic, sympathetic plus parasympathetic and the control group. The ability of antioxidation of blood from the subjects was measured with an ultraweak chemiluminescence analyzer. According to the results, the level of superoxide anions was decreased in sympathetic, parasympathetic, and sympathetic plus parasympathetic group, while that in the control group was increased. This suggested that the FIR radiation performed a significantly antioxidative effect by defending human from oxidative damage of superoxide anions in blood. This may probably be achieved by increasing SOD concentration and/or increasing heart rate variability. Keywords- Far-Infrared Radiation; Antioxidative Effect; Ultraweak Chemiluminescence Analyzer; Autonomic Nervous System; Superoxide Anions

Chun-Chih Lin1, Cheng-Lung Lee2, Chia-Chi Lung *3 1Department of Natural Biotechnology/Graduate Institute of Natural Healing Sciences/General education Center, Nanhua University, No.32, Chung Keng Li, Dalin, Chia-Yi 62248, Taiwan, R.O.C. 2Department of Criminal Investigation, Taiwan Police College, No.153, Sec. 3, Singlong Rd., Wunshan District, Taipei City 11696, Taiwan, R.O.C. *3Department of Public Health and Institute of Public Health, Chung-Shan Medical University/ Department of Family and Community Medicine, Chung Shan Medical University Hospital, No.110, Sec.1, Jianguo N.Rd., Taichung City 40201, Taiwan, R.O.C.


Infrared radiation is non-ionizing radiation emitted when a molecule de-excites from a higher vibrational or rotational quantum level, which physically expresses as heat [1-3]. In the infrared spectrum, the “growth rays” [4, 5] ranging of 4-14 μm belongs to far-infrared (FIR) spectrum, which is named ascribed to its many beneficial effects represented on organisms [6-9]. For thousands of years, FIR radiation has commonly been used in Chinese medicine to cure diseases by means of moxibustion [10, 11]. Moreover, FIR can also be expressed from qigong practicers, which has long been used to enhance health as well as to heal sickness in Chinese. Many biomedical materials serving growth rays, so called FIR materials, have recently been developed and manufactured for healthcare and clinical applications [12-16]. The emitted heat and radiation from the FIR materials can increase blood circulation, facilitate cell growth [6, 17], and tissue regeneration [18, 19], as well as inhibition of tumor growth [20, 21] and anti-depression [21, 22]. Sleep modulatory effect was also observed in rat under FIR irradiation [6]. On the other hand, positive effects of FIR were found helpful to several chronic diseases, such as joint pain, stiffness, knee osteoarthritis [23, 24], inflammation [25], limitation of muscle extension [26] and cancer [8]. Among the chronic diseases, many arise from damages of superoxide radicals, such as hyper pressure, Parkinson’s disease [27], arterial disease [28], hepatitis [29, 30] and others [30, 31]. In this research, we investigated the variation of the concentration of superoxide anions in blood of the recruited subjects treated by different arrangements of FIR hot compress to evaluate the antioxidative effect of FIR in human.

A. Study Population and Testing Environment
Forty-six students aged 18-30 years old were recruited from a university located in Chiayi County of Taiwan (R.O.C.) in this study, which was reviewed and approved by the institutional review board of Dalin Tzu Chi General Hospital in Taiwan (i.e., the approved informed consent was obtained). Written informed consents were returned from all subjects before carrying out the test. None of the recruited subjects possessed a family history of heart, inflammation symptoms or chronic diseases.
By stratified and random sampling with a computer, the volunteers were grouped into four experimental groups, including the sympathetic group (irradiated by FIR on thoracic lumbar vertebra; abbreviated as T; Fig. 1(A)), the parasympathetic group (irradiated by FIR on brain system and sacrum; abbreviated as P; Fig. 1(B)), as well as the sympathetic plus parasympathetic group (treated by FIR on brain system, thoracic lumbar vertebra, and sacrum; abbreviated as W; Fig. 1(C)). The control group was treated the same way as the experimental groups but without FIR irradiation to minimized placebo effect. It was confirmed that neither drug nor coffee-containing food was taken by the volunteers before the test. Volunteer that stayed up late at the night before the testing day was also screened out. The testing environment was quiet, comfortable, and well controlled at 20-
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25oC, 40-60% relative humidity and consistent lighting while performing the tests. Only one subject was evaluated at a time during the test. Fig. 1 Arrangements for the experimental groups: (A) the sympathetic group, (B) the parasympathetic group and (C) the sympathetic plus parasympathetic group

B. Equipment for FIR Generation
The FIR equipment obtained from Solano Semiconductor Technology Co., LTD. (R.O.C.) was manufactured as a compress pad with a dimension of 40 cm×28 cm×3 cm and the whole compress surface was embedded with ceramic FIR materials (emissivity=0.85). FIR emission was triggered by a 24 V power supply. Hot compress was implemented at different regions of the spine in different groups: T1-L2 for the sympathetic group; neck and epencephalon for the parasympathetic group; whole spine for the sympathetic plus parasympathetic group (Fig. 1). For the control group, whole spine was contacted to the compress but the power supply was turned off.

C. Sample Preparation and Analysis for Superoxide Anions in Blood
With the availability of an ultraweak chemiluminescence analyzer (BJL-1-IC; Jye Horn Co., Taiwan), the suppression of superoxide anions by the blood samples is possible to be monitored. Before FIR treatment, 2-3 mL peripheral blood was taken from each subject. Except for the control, the treatment of FIR was performed for 40 minutes following a stabilization period of 5-10 minutes. Another 2-3 mL of blood was sampled from the subject at the end of the test. All blood samples were kept at 37°C in the dark and analyzed within 24 hours after collected. An aliquot of 0.5-mL blood sample was pipetted into a glass tube and vortexed to mix. The half maximal inhibitory concentration (IC50) of the total blood against superoxide anions was determined from the change of chemiluminescence intensity. Being corrected for background, the obtained chemiluminescence intensity was represented in terms of average counts per minute.

D. Statistical Analysis
The distributions of characteristics among the testing groups were expressed as percentages for categorical variables and means for continuous variables. The association of categorical data was estimated by chi-square test. The paired t test was used to analyze the difference of concentration of superoxide anions among the groups. The results of each group were compared by a repeated measurement analysis of variances statistic method followed by the Schaffer test for post hoc analysis of significance. A P value <0.05 was considered statistically significant. SPSS version 12.0 was used for statistical analysis in this research.

Descriptive variables including gender and age are listed in Table 1. No significant difference among testing groups was observed from the distribution of demographic characteristics analyzed by chi-squared or one-way ANOVA. The concentration of superoxide anions in blood was previously indicated being influenced by age [26, 33-35]. Therefore, the subjects over 30 years old were excluded from the test to avoid the effect of age. Moreover, to evaluate the significance of decreased level among these groups, a decrease percentage of superoxide-anion level for the FIR-exposure groups was determined, which exhibited statistical significance as compared to the control group (Table 2). These results in this study reveal that FIR treatment can effectively reduce the generation of superoxide anions in blood. The changes of chemiluminescence intensity of the experimental groups before and after FIR irradiation was presented in Fig. 2. After FIR treatment as indicated by the result, the chemiluminescence intensity of the control group was increased, while that of the T, P, and W groups was decreased. This indicated that the concentration of superoxide anions in blood of the groups treated by FIR irradiation was eliminated.
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Number (%)
11 (24)
11 (24)
12 (26)
12 (26)
Gender (%)
6 (27)
5 (23)
5 (21)
6 (25)
6 (25)
7 (29)
Age (yr)
a chi-squared test b one-way ANOVA The abbreviation for Groups T, P and W respectively denotes the sympathetic, parasympathetic and sympathetic plus parasympathetic treatment group. TABLE II DIFFERENCE (AFTER MINUS BEFORE) OF SUPEROXIDE ANIONS BETWEEN BEFORE AND AFTER FIR TREATMENT IN EACH GROUP
Difference Mean(SD)
a pair t test b The group reached statistical significance in comparison with the control group (P < 0.05) by repeated analysis of variances method. The abbreviation for group T, P and W denotes the sympathetic, parasympathetic and sympathetic plus parasympathetic treatment group, respectively. The results were obtained from independently triplicate experiments. Control T P W02004006008001000Chemiluminescence intensity (
103)beforeafter Fig. 2 Variation for concentration of superoxide anions by means of chemiluminescence intensity before and after FIR treatment The abbreviation of T, P and W denotes the sympathetic, parasympathetic and sympathetic plus parasympathetic group, respectively. The results were obtained from independently triplicate experiments. Data are represented as box-and-whisker plot. The data are represented as box-and-whisker plot, which illustrate the smallest observation, lower quartile, median, upper quartile, and largest observation.
Superoxide anions are deleterious byproducts in mitochondrial respiration in organisms [32], which can poison energy metabolism and release potentially toxic iron by inactivating aconitase even at subnanomolar concentrations [36]. When microorganisms invades, the superoxide anions can also be released by immune system to destroy the invading pathogens (e.g., myriads of superoxide anions are produced by NADPH oxidase in phagocytes) [37, 38-40, 41-43] and causing inflammation symptoms [44]. From Table 2, all the experimental groups treated with FIR represented apparent antioxidative effect on decreasing the generation of superoxide anions, while an increased level of superoxide anions was observed in the control group. In this study, since none of the subjects had inflammation symptoms, the generation of superoxide anions should mainly be ascribed to mitochondrial respiration, and the variation of superoxide concentration could possibly be attributed to increase of superoxide dismutase (SOD), which is responsible for the reduction of superoxide anions in human [45-47]. Thermal as well as non-thermal effects (e.g., increase NO‧ concentration) of FIR have been proved able to cause vasodilatation and enhance blood circulation [48, 49] may increase metabolism of superoxide anions. According to previous researches [50, 51, 52], the simulation of FIR has been proved to be effective on increasing the production of SOD [27, 53]. In addition, the observed phenomena may also be ascribed to the regulation of autonomic nervous system since the generated heat from FIR irradiation has also been verified able to affect the autonomic nervous system and increase heart rate variability to
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eliminate superoxide anions [29, 54-56]. Moreover, we found that all of the hot-compress arrangements (i.e., different spine region of FIR irradiation in this study) exhibited positive effect on the elimination of superoxide anions. However, FIR irradiation on T1-L2 region (the sympathetic group) and whole spine (the sympathetic plus parasympathetic group) revealed better results. As the population lifetime prolongs worldwide, chronic diseases have become an important public health issue. From several studies, chronic diseases have been found arising from damage of superoxide anions [27-31, 57-59]. In this study, we propose that FIR treatment at the spine is beneficial for human in prevention from oxidative damage of superoxide anions. Therefore, the treatments of this study may provide an alternative strategy to prevent chronic diseases resulting from damage of superoxide anions in prevent medicine. However, there are limitations in this study. First, the sample size was limited. In the future, these results should be confirmed in a large sample size. Second, due to the first limitation, whether the results are statistically insignificant in gender when sample size in each group increases cannot be indicated from this study. Finally, the population of this study is relatively young; the findings may not be the same as those in old population. However, the results still propose that FIR treatment may have beneficial effects represented on old population and may be coordinated for health care as well as complimentary and alternative therapies in clinical applications.

This is the first study to assess the effects of FIR treatment on decreasing superoxide anions in human. Forty-six students aged 18-30 years old were recruited in this study to investigate the antioxidative effect of FIR in human by measuring the concentration of superoxide anions in blood of the recruited subjects receiving different arrangements of FIR hot compress. The results indicate that FIR treatment at the spine is effective in scavenging superoxide anions in blood, which merits further scientific investigations.

The authors acknowledge Solano Semiconductor Technology Co., Ltd. for the supply of equipment for FIR hot compress and Mr. Ying-Yeh Hsieh as well as Ms. Ming-Hua Fong for the assistance in the determination of superoxide concentration. The help of Dr. Moon-Sing Lee in obtaining the approval from institutional review board of Dalin Tzu Chi General Hospital is deeply appreciated.

No competing financial interests exist in this study.

[1] Y. J. Kaufman and U. P. Oppenheim, “Time-resolved molecular excitation and heat effects induced by infrared radiation,” Appl. Opt., vol. 16, pp. 1931-1935, Jul. 1977.
[2] M. Jackson, L. R. Zink, J. P. Towle, N. Riley, and J. M. Brown, “The rotational spectrum of the FeD radical in its X (4)Delta state, measured by far-infrared laser magnetic resonance,” J. Chem. Phys., vol. 130, pp. 154311, Apr. 2009.
[3] W. Karstens, D. C. Bobela, and D. Y. Smith, “Impurity and free-carrier effects on the far-infrared dispersion spectrum of silicon,” J. Opt. Soc. Am. A Opt. Image Sci. Vis., vol. 23, pp. 723-729, Mar. 2006.
[4] Y. Hamada, F. Teraoka, T. Matsumoto, A. Madachi, F. Toki, E. Uda, R. Hase, J. Takahashi, and N. Matsuura, “Effects of far infrared ray on Hela cells and WI-38 cells,” Int. Congress Series, vol. 1255, pp. 339-341, Aug. 2003.
[5] K. Ishi, Y. Shibata, T. Takahashi, H. Mishiro, T. Ohsaka, M. Ikezawa, Y. Kondo, T. Nakazato, S. Urasawa, N. Niimura, R. Kato, Y. Shibasaki, and M. Oyamada, “Spectrum of coherent synchrotron radiation in the far-infrared region,” Phys. Rev. A, vol. 43, pp. 5597-5604, May 1991.
[6] S. Inoue, and M. Kabaya, “Biological activities caused by far-infrared radiation,” Int. J. Biometeorol., vol. 33, pp. 145-150, Oct. 1989.
[7] C. C. Lin, C. F.Chang, M. Y. Lai, T. W. Chen, P. C. Lee, and W. C. Yang, “Far-Infrared Therapy: A Novel Treatment to Improve Access Blood Flow and Unassisted Patency of Arteriovenous Fistula in Hemodialysis Patients,” J. Am. Soc. Nephrol., vol. 18, pp. 985-992, Mar. 1989.
[8] S. Y. Yu, J. H. Chiu, S. D. Yang, Y. C. Hsu, W. Y. Lui, and C. W. Wu, “Biological effect of far-infrared therapy on increasing skin microcirculation in rats,” Photodermatol. Photoimmunol. Photomed., vol. 22, pp. 78-86, Apr. 2006.
[9] S. Cho, M. H. Shin, Y. K. Kim, J. E. Seo, Y. M. Lee, C. H. Park, and J. H. Chung, “Effects of infrared radiation and heat onhuman skin aging in vivo,” J. Investig. Dermatol. Symp. Proc., vol. 14, pp. 15-19, Jul. 2009.
[10] H. Wenxue, J. Jun, S. Jialin, X. Yonghong, and C. Jianhong, “Research on the measuring and duplication techniques of spectrum of the moxibustion in traditional chinese medicine,” Conf. Proc. IEEE Eng Med. Biol. Soc., vol. 4, pp. 4267-4270, 2005.
[11] C. C. Lu, “Chinese acupuncture and moxibustion,” Indian Med. J., vol. 56, pp. 54, Mar. 1962.
[12] M. A. Trelles, I. Allones, and E. Mayo, “Combined visible light and infrared light-emitting diode (LED) therapy enhances wound healing after laser ablative resurfacing of photodamaged facial skin,” Med. Laser Appl., vol. 21, pp. 165-175, Sep. 2006.
[13] J. T. Eells, M. T. T. Wong-Riley, J. VerHoeve, M. Henry, E. V. Buchman, M. P. Kane, L. J. Gould, R. Das, M. Jett, B. D. Hodgson, D. Margolis, and H. T. Whelan, “Mitochondrial signal transduction in accelerated wound and retinal healing by near-infrared light therapy,” Mitochondrion, vol. 4, pp. 559-567, Sep. 2004.
Journal of Public Health Frontier Jun. 2013, Vol. 2 Iss. 2, PP. 97-102
– 101 –
[14] A. Masuda, Y. Koga, M. Hattanmaru, S. Minagoe, and C. Tei, “The Effects of Repeated Thermal Therapy for Patients with Chronic Pain,” Psychother Psychosom, vol. 74, pp.288-294, Aug. 2005.
[15] L. C. Campbell, D. J. Clauw, and F. J. Keefe, “Persistent pain and depression,”: a biopsychosocial perspective,” Biol. Psychiat., vol. 54, pp. 399-409, Aug. 2003.
[16] L. R. Horwitz, T. J. Burke, and D. Carnegie, “Augmentation of wound healing using monochromatic infrared energy. Exploration of a new technology for wound management,” Adv. Wound. Care, vol. 12, pp. 35-40, Jan. 1999.
[17] R. Shiurba, T. Hirabayashi, S. Kiyokawa, A. Fukui, Y. Miyanaga, I. Kojima, and M. Asashima, “Evidence that far-infrared radiation promotes growth of Xenopus laevis,” Biol. Sci. Space, vol. 12, pp.3-4, Dec. 1998.
[18] H. Nagasawa, Y. Udagawa, and S. Kiyokawa, “Evidence that irradiation of far-infrared rays inhibits ammary tumor growth in SHN mice,” Anticancer Res., vol. 19, pp. 1797-1800, Jan. 1999.
[19] M. Segovia, F. J. Gordillo, and F. L. Figueroa, “Cyclic-AMP levels in the lichen Evernia prunastri are modulated by light quantity and quality,” J. Photochem. Photobiol. B: Biol., vol. 70, pp. 145-151, Jul, 2003.
[20] Y. Udagawa, H. Nagasawa, and S. Kiyokawa, “Inhibition by whole-body hyperthermia with far-infrared rays of the growth of spontaneous mammary turnours in mice,” Anticancer Res., vol 19, pp. 4125-4130, Sep. 1999.
[21] M. J. Bair, R. L. Robinson, W. Katon, and K. Kroenke, “Depression and pain comorbidity: a literature review,” Arch. Intern. Med., vol. 163, pp. 2433-2445, Nov. 2003.
[22] J. F. Tsai, S. Hsiao, and S. Y. Wang, “Infrared irradiation has potential antidepressant effect,” Prog.Neuro-Psychopharmacol. Biol. Psychiat., vol 31, pp. 1397–1400, Oct. 2007.
[23] S. A. Mazzuca, M.C. Page, R.D. Meldrum, K.D. Brandt, and S. Petty-Saphon, “Pilot study of the effects of a heat-retaining knee sleeve on joint pain, stiffness, and function in patients with knee osteoarthritis,” Arthritis Care & Res. vol 51, pp. 716–721, Oct. 2004.
[24] M. Usuba, Y. Miyanaga, S. Miyakawa, T. Maeshima, and Y. Shirasak, “Effect of Heat in Increasing the Range of Knee Motion After the Development of a Joint Contracture: An Experiment With an Animal Model,” Arch. Phys. Med. Rehabil. vol 87, pp. 247–253, Feb. 2006.
[25] Y. Shibata, N. Ogura, K. Yamashiro, S. Takashiba, T. Kondoh, K. Miyazawa, M. Matsui, and Y. Abiko, “Anti-inflammatory effect of linear polarized infrared irradiation on interleukin-1β-induced chemokine production in MH7A rheumatoid synovial cells,” Lasers in Med. Sci. vol 20, pp. 109-113, 2005.
[26] C.A. Knight, C.R. Rutledge, M.E. Cox, M. Acosta, and S.J. Hall, “Effect of Superficial Heat, Deep Heat, and Active Exercise Warm-up on the Extensibility of the Plantar Flexors,” Phys. Ther. vol 81, pp. 1206-1214, Jun 2001.
[27] D. J. Adams Jr., and I. N. Odunze, “Oxygen free radicals and Parkinson’s disease,” Free Radical. Biol. Med., vol. 10, pp. 161-169, Mar. 1991.
[28] J. J. F. Belch, M. Chopra, S. Hutchison, R. Lorimer, R. D. Sturrock, C. D. Forbes, and W. E. Smith, “Free radical pathology in chronic arterial disease,” Free Radical. Biol. Med., vol. 6, pp. 375-378, Jan. 1989.
[29] E. Larrea, O. Beloqui, M. A. Muñoz-Navas, M. P. Civeira, J. Prieto, “Superoxide Dismutase in Patients With Chronic Hepatitis C Virus Infection,” Free Radic. Biol. Med., vol. 24, pp. 1235-1241, May. 1998.
[30] N. J. Simmonds, “Free radicals in gastrointestinal and hepatic disease”, Immunopharmacology of Free Radical Species, D. Blake, and P. G. Winyard, Ed. San Diego, United State: Academic Press, 1995, pp.143-174.
[31] C. Ribiere, I. Hininger, C. Saffar-Boccara, D. Sabourault, and R. Nordmann, “Mitochondrial respiratory activity and superoxide radical generation in the liver, brain and heart after chronic ethanol intake,” Biochem. Pharmacol., vol. 47, pp. 1827-1833, May. 1994.
[32] H. C. Lee, and Y. H. Wei, “The role of mitochondria in human aging,” J. Biomed. Sci., vol 4, pp. 319-326, Apr. 1997.
[33] X. Xu, C. N. Chen, E. A. Arriaga, and L. V. Thompson, “Asymmetric superoxide release inside and outside the mitochondria in skeletal muscle under conditions of aging and disuse,” J. Appl. Physiol, vol. 109, pp. 1133-1139, Oct. 2010.
[34] A. Vanella, R. F. Villa, A. Gorini, A. Campisi, and A. M. Giuffrida-Stella, “Superoxide dismutase and cytochrome oxidase activities in light and heavy synaptic mitochondria from rat cerebral cortex during aging,” J. Neurosci. Res., vol. 22, pp. 351-355, Mar. 1989.
[35] C. Y. Lu, H. C. Lee, H. J. Fahn, and Y. H. Wei, “Oxidative damage elicited by imbalance of free radical scavenging enzymes is associated with large-scale mtDNA deletions in aging human skin,” Mutat. Res., vol. 423, pp. 11-21, Jan. 1999.
[36] U. Andersson, B. Leighton, M. E. Young, E. Blomstrand, and E. A. Newsholme, “Inactivation of aconitase and oxoglutarate dehydrogenase in skeletal muscle in vitro by superoxide anions and/or nitric oxide,” Biochem. Biophys. Res. Commun., vol. 249, pp. 512-516, Aug. 1998.
[37] J. F. Turrens, “Superoxide Production by the Mitochondrial Respiratory Chain,” Biosci. Rep., vol 17, pp. 3-8, 1997.
[38] E. N. Churchill and L. I. Szweda, “Translocation of deltaPKC to mitochondria during cardiac reperfusion enhances superoxide anion production and induces loss in mitochondrial function,” Arch. Biochem. Biophys., vol. 439, pp. 194-199, July 2005.
[39] M. C. Plotkowski, H. C. Povoa, J. M. Zahm, G. Lizard, G. M. Pereira, J. M. Tournier, and E. Puchelle, “Early mitochondrial dysfunction, superoxide anion production, and DNA degradation are associated with non-apoptotic death of human airway epithelial cells induced by Pseudomonas aeruginosa exotoxin A,” Am. J. Respir. Cell Mol. Biol., vol. 26, pp. 617-626, May 2002.
[40] D. Han, F. Antunes, F. Daneri, and E. Cadenas, “Mitochondrial superoxide anion production and release into intermembrane space,” Methods Enzymol., vol. 349, pp. 271-280, 2002.
[41] A. Shiryaeva, A. Arkadyeva, L. Emelyanova, G. Sakuta, and V. Morozov, “Superoxide anion production by the mitochondrial respiratory chain of hepatocytes of rats with experimental toxic hepatitis,” J Bioenerg. Biomembr. vol 41, pp. 379-385, Oct. 2009.
[42] P. G. Gervasi, M. R. Agrillo, L. Citti, R. Danesi, and T. M. Del, “Superoxide anion production by adriamycinol from cardiac sarcosomes and by mitochondrial NADH dehydrogenase,” Anticancer Res., vol. 6, pp. 1231-1235, Sep.1986.
Journal of Public Health Frontier Jun. 2013, Vol. 2 Iss. 2, PP. 97-102
– 102 –
[43] P. G. Gervasi, M. R. Agrillo, A. Lippi, N. Bernardini, R. Danesi, and T. M. Del, “Superoxide anion production by doxorubicin analogs in heart sarcosomes and by mitochondrial NADH dehydrogenase,” Res. Commun. Chem. Pathol. Pharmacol., vol. 67, pp. 101-115, Jan. 1990.
[44] M McCord, and RS Roy, “The pathophysiology of superoxide: roles in inflammation and ischemia,” Can. J. Physiol. Pharmacol. 60, pp.1346-1352, Nov. 1982.
[45] S. I. Liochev, and I. Fridovich, “The effects of superoxide dismutase on H2O2 formation,” Free Radical. Biol. Med., vol 42, pp. 1465-1469, Feb. 2007.
[46] M. A. Secilmis, O. E. Kiroglu, and N. Ogulener, “Role of superoxide dismutase enzymes and ascorbate in protection of nitrergic relaxation against superoxide anions in mouse duodenum,” Acta Pharmacol. Sin., vol. 29, pp. 687-697, Jun. 2008.
[47] S. N. Hawk, L. Lanoue, C. L. Keen, C. L. Kwik-Uribe, R. B. Rucker, and J. Y. Uriu-Adams, “Copper-deficient rat embryos are characterized by low superoxide dismutase activity and elevated superoxide anions,” Biol. Reprod., vol. 68, pp. 896-903, Mar. 2003.
[48] R. Beever, “Far-infrared saunas for treatment of cardiovascular risk factors,” Can. Fam. Physician vol. 55, pp. 691-696, Jul. 2009.
[49] M. Imamura, S. Biro, T. Kihara, S. Yoshifuku, K. Takasaki, Y. Otsuji, S. Minagoe, Y. Toyama, and C. Tei, “Repeated thermal therapy improves impaired vascular endothelial function in patients with coronary risk factors,” J. Am. Coll. Cardiol., vol. 38, pp. 1083-1088 Oct. 2001.
[50] Y. Niwa, “Oxidative injury and its defense system in vivo,” Rinsho Byori., vol 47, pp. 189-209, Mar. 1999.
[51] K. I. Jeon, E. Park, H. R. Park, Y. J. Jeon, S. H. Cha, and S. C. Lee, “Antioxidant activity of far-infrared radiated rice hull extracts on reactive oxygen species scavenging and oxidative DNA damage in human lymphocytes,” J. Med. Food, vol. 9, pp. 42-48, 2006.
[52] J. F. Lee, “A Complementary Therapy of Far-Infrared-Ray Hot Compression for the Elderly Patients with Type II Diabetes Mellitus,” M. Chin. thesis, Nanhua University, Taiwan, R.O.C., Jun. 2010.
[53] R. A. Greenwald, “Superoxide dismutase and catalase as therapeutic agents for human diseases a critical review,” Free Radical. Biol. Med., vol. 8, pp. 201-209, Jan. 1990.
[54] J. Thireau, D. Poisson, B. L. Zhang, L. Gillet, P. M. Le, C. Andres, J. London, and D. Babuty, “Increased heart rate variability in mice overexpressing the Cu/Zn superoxide dismutase,” Free Radic. Biol. Med., vol. 45, pp. 396-403, Aug. 2008.
[55] L. Gao, W. Wang, Y. L. Li, H. D. Schultz, D. Liu, K. G. Cornish, and I. H. Zucker, “Superoxide mediates sympathoexcitation in heart failure: roles of angiotensin II and NAD(P)H oxidase,” Circ. Res., vol. 95, pp. 937-944, Oct. 2004.
[56] C. T. Hsu, “The role of the autonomic nervous system in chemically-induced liver damage and repair–using the essential hypertensive animal model (SHR),” J. Auton. Nerv. Syst., vol. 51, pp. 135-142, Feb. 1995.
[57] D. J. Volkman, E. S. Buescher, J. I. Gallin and A. S. Fauci, “B cell lines as models for inherited phagocytic diseases: abnormal superoxide generation in chronic granulomatous disease and giant granules in Chediak-Higashi syndrome,” J. Immunol., vol 133, pp. 3006-3009, Jan., 1984.
[58] B. Halliwell, “Production of superoxide, hydrogen peroxide and hydroxyl radicals by phagocytic cells: A cause of chronic inflammatory disease?” Cell Biol. Intr. Rep., vol. 6, pp. 529-542, Jun. 1982.
[59] J. K. Willcox, S. L. Ash and G. L. Catignani, “Antioxidants and Prevention of Chronic Disease,” Crit. Rev. Food Sci., vol 44, pp. 275-295, Aug., 2004.