the effect of radiation on thyroid gland

Abstract

Abstract
Radiation emitted from sources that are transmitted through an intermediated medium and absorbed by animal body. Radiation is very high up environmental toxin. Many sources of radiations are mobile phone, computer, UV lamp and torches radiation affected animal’s body organs such as thyroid gland, liver, kidney, etc. Radiations cause oxidative stress and generate free radicals such as hydroxyl radical, superoxide, nitric oxide, hydrogen peroxide radicals etc. These free radicals are unstable and chemically very active acting as an oxidizing agent that causes the morphological and physiological changes in the cells. In thyroid cells, these radicals can contact the other macromolecules and increase to changes in their structure and functions and hypo or hyperthyroidism conditions. An antioxidant our well wisher of damaging cells. Antioxidants inhibit the generation of free radicals and protect the cells. Antioxidants are essential for many enzymatic reactions and also acts as a free radical scavenger.
Keywords: radiation, thyroid gland, oxidative stress, antioxidants

Full text

International Journal of Biology Research
217
International Journal of Biology Research
ISSN: 2455-6548
Impact Factor: RJIF 5.22
www.biologyjournal.in
Volume 3; Issue 1; January 2018; Page No. 217-222
The effect of radiation on thyroid gland
Gayatri Rai, Arun Kumar, * Dr. Payal Mahobiya
Department of Zoology, Dr Harisingh Gour Vishwavidhyalaya, (A Central University), Sagar, Madhya Pradesh, India
Abstract
Radiation emitted from sources that are transmitted through an intermediated medium and absorbed by animal body. Radiation is
very high up environmental toxin. Many sources of radiations are mobile phone, computer, UV lamp and torches radiation affected
animal’s body organs such as thyroid gland, liver, kidney, etc. Radiations cause oxidative stress and generate free radicals such as
hydroxyl radical, superoxide, nitric oxide, hydrogen peroxide radicals etc. These free radicals are unstable and chemically very
active acting as an oxidizing agent that causes the morphological and physiological changes in the cells. In thyroid cells, these
radicals can contact the other macromolecules and increase to changes in their structure and functions and hypo or
hyperthyroidism conditions. An antioxidant our well wisher of damaging cells. Antioxidants inhibit the generation of free radicals
and protect the cells. Antioxidants are essential for many enzymatic reactions and also acts as a free radical scavenger.
Keywords: radiation, thyroid gland, oxidative stress, antioxidants
1. Introduction
People are affected by radiation from different sources.
Energy emitted from a source that is transmitted through an
intermediate medium and absorbed by the animal body.
Radiation is very high up environmental toxin and
transmission of energy in the form of particles or
waves through sources. Radiation impression of the ionizing
and non-ionizing radiation. Even though ionizing and non-
ionizing radiation has been used extensively in the many
sources such as a mercury lamp, dental polymerizing
equipment, X-rays machine, black light lamp, welding
equipment, counterfeit currency detectors, etc. Consequently,
radiation effect on the body organs such as the thyroid gland
[1, 2], eyes [3], liver [4], skin [5]. The UV radiation is
electromagnetic radiation and maximum generated from
sunlight. UV radiation is a non-ionizing and classified into
three types UV-C, UV-B & UV-A. UV-C (200-280 nm,
shortwave) is lethal than UV-B (280-320nm, medium wave).
It causes skin darkening and erythema, the skin cancer
possibility increases from long exposure to UV-B, UV-A is
non-lethal radiation (320-400 nm, long wave). UV radiation
damage cells and produced free radicals. Ionizing radiations
having high energy and short wavelength. It include X-rays,
gamma rays, alpha and beta particles. Ionizing radiation has
enough energy to generate ions. Which damage the cells,
enzymes, protein and nucleic acid [6, 7, 8].
Fig 1: Types of UV Radiation
The thyroid gland is the largest endocrine gland and consists
of two lobes beside the trachea and lowers the larynx. The
thyroid gland secretes the thyroid hormones which influence
the basal metabolic rate, protein synthesis and have a wide
range of other effects including on the development,
respectively. The thyroid hormones T3 and T4 are synthesized
from iodine and tyrosine in follicle cells. The thyroid also
produces calcitonin hormones; it plays a role in calcium
homeostasis.
Radiation generates the oxidative stress, Oxidative stress
founded when the imbalance between reactive oxygen species
(ROS) and antioxidants and cells tried to work against the
oxidant property and redox balance through the stimulation of
defensive enzymes, proteins [9, 10]. Even though oxidative
reactions arise in all tissues and organs, the thyroid gland
mobilizes such an organ in which oxidative processes are
essential for thyroid hormone synthesis. It is Putative that vast
quantity of ROS, particularly of hydrogen peroxide (H2O2),
are yield in the thyroid underneath physiological conditions.
Yet, with extra oxidative misuse caused by ionizing radiation,
improved damage to macromolecules occurs, potentially
leading to different thyroid diseases, also, cancer involved [11].
Non-ionizing radiation shows noxious effect of the thyroid
gland. This generates the free radicals. A radical is groups of
molecule that containing one or more unpaired electrons [12].
Free radicals generated by our body from a different type of
radiation. If free radicals extreme the body's capability to
control them, a situation known as oxidative stress. Free
radicals thus harmfully vary lipids, proteins, and DNA and
generate a number of human diseases [13]. There are many
types of radicals, but those of main concern in biological
systems are derived from oxygen, it called reactive oxygen
species. Superoxide anion, hydrogen peroxide, hydroxyl
radical is also reactive oxygen species. The Modern growth in
the information of free radicals and reactive oxygen species

International Journal of Biology Research
218
(ROS) in biology is Procreating a medical revolution that
promises a new age of health and disease administration [14].
Reactive oxygen species are also formed during the
metabolism of oxygen.
The noxious effect of ionizing radiation in natural systems are
mostly mediated through the generation of reactive oxygen
species (ROS) in cells as a result of water radiolysis [15],
render rise to OH- and H+ [8]. Ionizing radiation interacts with
biological systems to encourage the extreme flow of free
radicals that attack different cellular elements [16]. The effect
of ionizing radiation on the thyroid is well recognized [17]. The
pathophysiological description of radiation-induced thyroid
damage is related to inhibition of follicular epithelial function
and subsequent progressive alteration of the endothelium, the
effect increases by time [18, 19]. The possibility of thyroid
carcinoma after exposure to radiation doses higher than 0.05 -
0.1 Gy is higher in younger children at the time of exposure
and all efforts should be performed to avoid some radiation
exposure during childhood [20]. Several thyroid abnormalities
may be caused by radiation exposure [21].
Reactive oxygen species (ROS) together with partially
reduced forms of oxygen i.e. superoxide anion, hydrogen
peroxide and hydroxyl radical as well as organic counterparts
such as lipid peroxides are produced as natural consequences
of oxidative cell metabolism. Under physiological conditions,
ROS [22] generation is controlled by a large number of anti-
free radical systems which act as protective mechanisms.
These systems consist of antioxidant enzymes such as
superoxide dismutase, catalase, glutathione peroxidase, and
glutathione reductase as well as non-enzymatic antioxidants,
among which the most important vitamins C and E,
carotenoids, and glutathione. Interruption of the antioxidant
stability results since the increased generation of ROS,
inactivation of detoxification systems, or excessive
exploitation of antioxidants. The disturbance is a causative
factor in the oxidative damage of cellular structures and
molecules such as lipids, proteins, and nucleic acids [23].
The aim of present reviewed the effect of UV-radiation on the
thyroid gland and their oxidative effect of rats, the study of
preventive effects of antioxidant on rat thyroid activities.
2. Radiations
Radiations are an energy source, transmitted through a source
have sufficient energy to penetrate living and non-living cells.
Radiations are found in many forms and affected by the
natural environment and yield through recent technology.
Mostly radiations have the potential for both effects positive
and negative. Radiation-induced damage might result in
adverse health effects within hours to weeks and delayed
effects may be observable many months after exposure [4].
Even though sunlight very essential radiation of the entire can
be detrimental in extreme amounts. Basically, radiation
classified into two categories ionizing and non-ionizing.
Ionizing and non-ionizing radiation exerts its effects on the
thyroid gland, involving long-term damage cancer, both
radiations mostly targeted of several genes, protein, lipids and
cause cancer [24].
3. Thyroid and Ionizing Radiation
Ionizing radiation is not detected by any of our senses but can
be easily detected by electronic equipment. Ionizing radiation
is emitted by radioactive atoms. Its energy is high enough to
damage our bodies. Actuality, Ionizing radiation energy in the
form of waves or particles that has as much as a necessary
force to eliminate electrons from atoms. The quantity of
ionizing radiation that can be rendered to treat tumours are
limited due to the nearby normal tissues and organs in the
Proximity of a tumour that could be also exposed to the
radiation causing damage [25]. In humans and animals, ionizing
radiation may cause cancer, death, and failure of neural
function and also stimulate mutation, chromosomal
aberrations and apoptosis in cells [26, 27]. Ionizing radiation has
enough energy to generate ions. Ionizing radiations damage
the cells, enzymes, protein and nucleic acid [6, 7, 8].
He–Ne laser has a potential therapeutic performance to
ameliorate the damaging effect of the ionizing radiation,
which depends on the frequency of its application. Further
studies with longer periods of treatment are recommended [28].
Even though oxidative reactions take place in all tissues and
organs, the thyroid gland constitutes such an organ in which
oxidative processes are indispensable for thyroid hormone
synthesis. It is estimated that huge amount of reactive oxygen
species, particularly of H2O2, are formed in the thyroid under
the physiological situation. Yet, with additional oxidative
mistreatment caused by IR, increased damage to
macromolecules occurs, potentially leading to different
thyroid diseases, cancer included [9].
4. Thyroid and Non-ionizing Radiation
Non-ionizing radiations are longer wavelength and low
energy. This radiation included UV radiation, visible light,
infrared; microwave, radiowave and these radiations are using
a Computer monitor, photocopier machine, printers, and
mercury lamps. Thyroid gland of rat exposed by exposure to
2.45 GHz radiation and obtained the glandular hypertrophy
in relation to the SAR and changes of the distribution of HSP-
90 linked with membranes and parafollicular cells and these
effects might not be absolutely formed by radiation and the
hypothalamus can be included with another indirect effect [29].
Table 1: Types of Non-Ionizing Radiation and their Wavelength
S. No
Non-Ionizing Radiation
Wavelength
1.
Ultraviolet
200-400nm
2.
Visible light
400-700nm
3.
Infrared
750nm-1m
4.
Microwave
1mm-1m
5.
Radiowave
1mm -100km
The thyroid gland is sensitive to EMF exposure and this
exposure induced morphological changes with drop off in
serum T4 and T3. These changes remained to the end of the
experiment indicating that a longer period of time is required
for the return of normal thyroid activity after EMF exposure.
Besides, the results revealed significant improvement in the
supervision of vitamin E through the exposure time [30].
5. Thyroid and UV Radiation
The UV radiations are major factors for set-up and
development of UV-initiated disease and Sunburn. [31, 32]
Prolonged exposure to solar-simulated UV irradiation leads to

International Journal of Biology Research
219
gathering of free radicals in the skin [33], immune suppression
and synthesis of excessive proinflammatory cytokines, all
resulting in oxidative stress in different tissues [34, 35]. UV
irradiation is known to induce apoptosis in many cell types [36,
37]. UV irradiation causes direct DNA damage (thymine
dimers) and forms bulky adducts that cause structural
distortion in the normal double-strand DNA backbone [38]. UV
irradiation could also diminish the intracellular content of
reduced glutathione [39] possibly through peroxidation of
lipids, causing the production of free hydroxyl radicals and a
state of oxidative stress in the cell; the resulting damage
occurs in proteins, lipids, and DNA. UV radiation exerts its
effects on the thyroid gland; involving long-term exposure
radiations mostly target several genes, protein, lipids and
causes cancer [21].
Fig 2: Exposure to UV radiation on rat and thyroid dysfunction by
the generation of free radicals.
Thyroid hormones are implicated in the control over the
oxidative stress in a very difficult way and the pre-exposition
to UV radiation tends to initiate oxidative stress in tissues, the
question arises about the effect of the prolonged exposition to
UV radiation on animals with hypothyroidism [40]. Ultraviolet
radiation was shown to induce a dose-dependent activation of
the apoptotic process in FTRL-5 cells cultured in the presence
of TSH [41, 42]. In the same cells flown in a stratospheric
balloon, a similar effect appeared to be the result of
modifications of the nuclear lipid metabolism, that is,
augmentation of sphingomyelin degradation and
phosphatidylcholine synthesis [43]. Acute and long-term
clinical manifestations of radiation exposure include the
development of cataracts; damage to the central nervous
system, gastrointestinal tract, skeletal system, and blood-
forming organs; and increased cancer risk. At high doses, it
also becomes an immediate threat to life. Different studies
have evaluated the plasma levels of key hormones involved in
the regulation of fluid volume, electrolyte concentrations, and
energetic metabolism in spaceflights conditions and have
found multiple changes in the response of the endocrine
system [44], Among these, functional alterations of the thyroid
suggestive of hypothyroidism have been documented in both
animals and humans [45, 46, 47, 48, 49, 43, 50, 51]. In particular,
decreased triiodothyronine (T3) and elevated thyroid-
stimulating hormone (TSH) plasma levels have been detected
in astronauts during spaceflights compared with prefight
values, and both hormones returned to the normal level in the
postflight period. Similarly, decreased thyroxine (T4) and T3
plasma concentrations have been shown in rats flown aboard a
biosatellite, together with morphological and histochemical
changes consistent with reduced thyroid activity, that is,
significant reduction of thyrocyte size, accumulation of colloid
drops in the cytoplasm, decrease of iodinated thyroglobulin in
the colloid, and lower T4 and T3 content per unit of thyroid
tissue mass [52].
The thyrotropin receptor is preferentially coupled to the alpha
subunit of the stimulatory guanine nucleotide binding protein
(Gsα) that activates adenylate cyclase and increases the
accumulation of cyclic AMP (cAMP). At higher thyrotropin
concentrations, the receptor also couples to the q subunit of
guaninenucleotide–binding protein alpha, resulting in the
activation of phospholipase C, and there is recent evidence
that the receptor may be coupled to members of other G
protein families [53]. In addition, insulin-like growth factor I,
epidermal growth factor, transforming growth factor β,
platelet-derived growth factor, fibroblast growth factor, and
cytokines, mainly acting by means of the protein tyrosine
kinase signal transduction pathway, stimulate the growth and
de differentiation of thyroid epithelial cells [54]. The growth
and function of the thyroid are stimulated by cAMP [54, 55].
This second messenger indirectly regulates the expression of
the thyroglobulin and thyroid peroxidase genes, whose
promoters contain binding sites for the transcription factors
TTF1, TTF2, and PAX8 [56]. As a consequence, continued
stimulation of the cAMP pathway causes hyperthyroidism
(Fig. 3).
Hypothyroidism may develop in patients with cutaneous T-
cell lymphoma who are treated with high-dose bexarotene,
most likely because the retinoid X receptor-selective ligand
suppresses thyrotropin secretion. Retinoid X receptor–
selective ligands can suppress thyrotropin secretion, resulting
in central hypothyroidism [57].

International Journal of Biology Research
220
Fig 3: TSH receptor coupled to cAMP and regulated the hyperthyroidism and cell proliferation
6. Radiations and Antioxidants
An antioxidant our well-wisher of damaging cells.
Antioxidants inhibit the generation of free radicals and protect
the cells. Antioxidants are essential for many enzymatic
reactions and also acts as a free radical scavenger. the
administration of antioxidants namely Vitamin C, Vitamin E
and turmeric significantly increased in the circulating levels of
T3 and T4 and this hormones responded to antioxidants
representing the significance of antioxidants for the prevention
of occurrence of certain diseases in thyroid gland by
protecting biological system against potentially harmful
effects of processes or reactions that can cause excessive
oxidations [58].
7. Conclusion
This review looks at the generation of free radicals by the
radiation i.e. ionizing and non-ionizing radiations. Ionizing
radiation like x-rays, gamma rays and non-ionizing radiation
especially UV radiation generate the free radicals and
oxidative stress in the thyroid gland and determined changes
in thyroid hormones and their functions. Thyroid hormones
are implicated in the control over the oxidative stress in a very
difficult way and the pre-exposition to UV radiation tends to
initiate oxidative stress in tissues and the effect of the
prolonged exposition to UV radiation on animals with
hypothyroidism. Many receptors involved the thyroid
dysfunctions such as retinoid X receptor-selective ligands can
suppress thyrotropin secretion, resulting in central
hypothyroidism and TSH receptor (thyrotropin receptor) is
coupled mainly to the cAMP pathway by means of the alpha
subunit of the stimulatory guanine nucleotide binding protein.
The cAMP regulates the manufacture of thyroid hormone and
the proliferation of thyroid epithelial cells and thereby
mediates hyperthyroidism.
8. Acknowledgments
Authors thanks, Department of Zoology, Dr Harisingh Gour
Central University Sagar (M.P.), India for providing
infrastructural facilities and constant support and UGC-RGNF
for financial support.
9. References
1. Walters OM, Anson BJ, Ivy AC. The effect of X-rays on
the thyroid and parathyroid glands. Radiology, 1930, 52-
58.
2. Esmekaya MA, Seyhan N, Omeroglu S. Pulse modulated
900 MHz radiation induces hypothyroidism and apoptosis
in thyroid cells: A light, electron microscopy and
immunohistochemical study. Int J Radiat Biol. 2010;
86(12):1106-1116.
3. Balci M, Namuslu M, Devrim E, Durak I. Effect of
Computer Monitor-Emitted Radiation on
Oxidant/Antioxidant Balance in Cornea and Lens from
Rats. Molecular Vision. 2009; 15:2521-2525.
4. Gultekin FA, Bakkal BH, Guven B, Tasdoven I, Bektas S,
Can M et al. Effects of ozone oxidative preconditioning
on radiation-induced organ damage in rats. J Radiat Res.
2013; 54(1):36-44.
5. Matsumura Y, Ananthaswamy HN. Toxic effects of
ultraviolet radiation on the skin. Toxicology and Applied
Pharmacology. 2004; 195:298-308.
6. Lett JT. Damage to cellular DNA from particulate
radiations, the efficacy of its processing and the
radiosensitivity of mammalian cells. Emphasis on DNA
strand breaks and chromatin breaks. Radiat Environ
Biophys. 1992; 31:257-277.
7. Daniniak N, Tann BJ. The utility of biological
membranes as indicators for radiation exposure:
alterations in membrane structure and function over time.
Stem Cells. 1995; 13:142-152.
8. Kamat JP, Boloor KK, Devasagayam TPA,
Venkatachalam SR. Antioxidant properties of Asparagus
racemosus against damage induced by gamma-radiation
in rat liver mitochondria. J Ethnopharmacol. 2000;
71:425-435.
9. Dalton TP, Shertzer HG, Puga A. Regulation of gene
expression by reactive oxygen. Ann Rev Pharmacol
Toxicol. 1999; 39:67-101.
10. Scandalios JG. Genomic responses to oxidative stress. In:
Meyers RA, Encyclopedia of Molecular Cell Biology and
Molecular Medicine. 2004; 5:489-512.
11. Karbownik-Lewinska M, Kokoszko-Bilska A. Oxidative
damage to macromolecules in the thyroid Experimental

International Journal of Biology Research
221
evidence. Thyroid Res. 2012; 5(1):25-27.
12. Finkel T, Holbrook NJ. Oxidants, oxidative stress and
the biology of ageing. Nature. 2000; 408:239-247.
13. Lobo V, Patil A, Phatak A, Chandra N. Free radicals,
antioxidants and functional foods: Impact on human
health. Pharmacogn Rev. 2010; 4(8):118-126.
14. Aruoma OI. Methodological consideration for
characterization of potential antioxidant actions of
bioactive components in plant foods. Mutat Res. 2003;
532:9-20.
15. Barakat IA, Abbas OA, Ayad S, Hassan AM. Evaluation
of radioprotective effects of wheat germ oil in male rats. J
Am Sci. 2011; 7(2):664-673.
16. Shirazi A, Mihandoost E, Ghobadi G, Mohseniand M,
Ghazi-Khansari M. Evaluation of the radioprotective
effect of melatonin on whole body irradiation induced
liver tissue damage. Cell J. 2013; 14(4):292-299.
17. Laulund AS, Nybo M, Brix TH, Abrahamsen B,
Jorgensen HL, Hegedeus L. Duration of thyroid
dysfunction correlates with all-cause morta lity. The
OPENTHYRO Register Cohort. 2014; PLoS One 9(10):
e110437.
18. Jung JH, Jung J, Kim SK, Woo SH, Kang KM, Jeong BK
et al. Alpha-lipoic acid attenuates radiation-induced
thyroid injury in rats. 2014; PLoS One 9(11):e112253. 29.
19. Simoes-Pereira J, Silva-Vieira M, Pereira MC. Latency
period until the development of thyroid cancer in young
patients submitted to radiotherapy: Report of 10 cases.
Case Rep Oncol. 2014; 7:810-814.
20. Iglesias ML, Schmidt A, Ghuzlan AA, Lacroix L, De
Vathaire F, Chevillard V et al. Radiation exposure and
thyroid cancer: a review. Arch Endocrinol Metab. 2017;
61(2):180-187.
21. Sinnott B, Ron E, Schneider AB. Exposing the thyroid to
radiation: a review of its current extent, risks, and
implications. Endocr Rev. 2010; 31(5):756-773.
22. Komosinska-Vassev K, Olczyk K, Kucharz EJ, Marcisz
C, Winsz-Szczotka K, Kotulska A. Free radical activity
and antioxidant defense mechanisms in patients with
hyperthyroidism due to Graves disease during therapy.
Clinica Chimica Acta. 2000; 300:107-117.
23. Kehrer JP. Free radicals as mediators of tissue injury and
disease. Crit. Rev. Toxicol. 1993; 23:21-48.
24. Albi E, Cataldi S, Lazzarini A, Codini M, Beccari T,
Ambesi-Impiombato FS et al. Radiation and Cancer. Int J
Mol Sci. 2017; 18:1-11.
25. Kunwar A, Bansal P, Kumar SJ, Bag PP, Paul P, Reddy
ND et al. In vivo radioprotection studies of 3,
3’diselenodipropionic acid, a selenocysteine derivative.
Free Radical Biology & Medicine. 2010; 48:399-410.
26. Nair CK, DK-Parida DK, T-Nomura T. Radioprotectors
in radiotherapy. J Radiat Res. 2001; 42:21-37.
27. Jagetia GC, Reddy TK. Modulation of radiation-induced
alteration in the antioxidant status of mice by naringin.
Life Science. 2005; 77:780-794.
28. Morcos N, Omran M, Hala Ghanem H, Elahdal M, Kamel
N, Attia E. Phototherapeutic Effect of Low-Level Laser
on Thyroid Gland of Gamma-Irradiated Rats.
Photochemistry and Photobiology. 2015; 91:942-951.
29. Agustino MJM, Jorge-Mora T, Jorge-Barreiro FJ, Suarez-
Quintanilla J, Moreno-Piquero E, Ares-Pena FJ et al.
Exposure to non-ionizing radiation provokes changes in
rat thyroid morphology and expression of HSP-90. Exp.
Bio. Med. 2015, 1-13.
30. Mohamed DA, Elnegris HM. Histological Study of
Thyroid Gland after Experimental Exposure to Low-
Frequency Electromagnetic Fields in Adult Male Albino
Rat and Possible Protective Role of Vitamin E. J Cytol
Histol. 2015; 6(6):1-8.
31. Singh RK, Gutman M, Reich RM. Ultraviolet B
Irradiation Promotes Tumorigenic and Metastatic
Properties in Primary Cutaneous Melanoma via Induction
of Interleukin 81. Cancer Research. 1995; 55:3669-3674.
32. Bald T, Quast T, Landsberg J, Rogava M, Glodde N,
Lopez-Ramos D et al. Ultraviolet-radiation-induced
inflammation promotes angiotropism and metastasis in
melanoma. Nature. 2014; 507:109-128.
33. Wagener FA, Carels CE, Lundvig DM. Targeting the
redox balance in inflammatory skin condition Int. J.
Molecular Science. 2013; 14:9126-9167.
34. Wei H, Zhang X, Wang YM. Inhibition of ultraviolet
light-induced oxidative events in the skin and internal
organs of hairless mice by isoflavone genistein. Cancer
Lett. 2002; 185:21-29.
35. Halliday GM, Damian DL, Rana S, Byrne SN. The
suppressive effects of ultraviolet radiation on immunity in
the skin and internal organs: Implications for
autoimmunity. J. Dermatology Science. 2012; 66:176-
182.
36. Godar DE, Lucas AD. Spectral dependence of UV-
induced immediate and delayed apoptosis: The role of
membrane and DNA damage. Photochem Photobiol.
1995; 62:108-113.
37. Radziszewska E, Piwocka K, Skierski J, Sikora E. UVC-
induced cell death of IL-2-dependent human
lymphocytes. Cell Biol Int. 1999; 23:97-103.
38. Sarasin A, Bounacer A, Lepage F, Schlumberger M,
Guillermo-Suarez H. Mechanisms of mutagenesis in
mammalian cells Application to human thyroid tumours.
CR Acad Sci III, 1999; 322:143-149.
39. Lautier D, Luscher P, Tyrrel RM. Endogenous
glutathione levels modulate both Constitutive and UV-A
radiation/hydrogen peroxide inducible expression of the
human heme oxygenase gene. Carcinogenesis. 1992;
13:227-232.
40. Valcheva-Traykova ML, Bocheva GS. Effect of
ultraviolet radiation on the free Radical’s formation in
hypothyroid rat’s liver. Bulgarian Chemical
Communications. 2016; 48(3):384-388.
41. Meli A, Perrella G, Curcio F, Ambesi-Impiombato F. In
vitro cultured cells as probes for space radiation effects
on biological systems. Mutat Res. 1999b; 430:229-234.
42. Del Terra E, Francesconi A, Donnini D, Curcio F,
Ambesi-Impiombato FS. Thyrotropin effects on
ultraviolet radiation-dependent apoptosis in FRTL-5 cells.
Thyroid. 2003; 13:747-753.
43. Albi E, Cataldi S, Villani M, Perrella G. Nuclear
phosphatidylcholine and Sphingomyelin metabolism of
thyroid cells changes during stratospheric balloon flight. J
Biomed Biotechnol. 2009, 1-5.

International Journal of Biology Research
222
44. Lane HW, Feeback DL. Water and energy dietary
requirements and endocrinology of Human space flight.
Nutrition. 2002; 18:820-828.
45. Stein TP, Schluter MD, Moldawer LL. Endocrine
relationships during human spaceflight. Am J Physiol
Endocrinol Metab. 1999; 276:155-162.
46. Strollo F. Hormonal changes in human spaceflights. Adv
Space Biol Med. 1999; 7:99-129.
47. Grindeland RE, Dotsenko MA, Mukku VR, Bigbee AJ,
Bengston SG. Rhesus monkey hormonal responses to
microgravity. J Gravit Physiol. 2000; 7:143.
48. McMonigal KA, Braverman LE, Dunn JT, Stanbury JB,
Wear ML, Hamm PB et al. Thyroid function changes
related to use of iodinated water in the U.S. space
program. Aviat Space Environ Med. 2000; 71:1120-1125.
49. Macho L, Kvetnansky R, Fickova M, Popova IA,
Grigoriev A. Effects of exposure to Spaceflights on
endocrine regulations in experimental animals. Endocr
Regul. 2001; 35:101-114.
50. Hellweg, CE, Baumstark-Khan C. Getting ready for the
manned mission to Mars: the astronauts’ risk from space
radiation. Naturwissenschaften. 2007; 94:517-526.
51. Dayanandan P. Gravitational biology and space life
sciences: current status and implications for the Indian
space programme. J Biosci. 2011; 36:911-919.
52. Plakhuta-Plakutina GI, Kabitskil EN, Dmitrieva NP,
Amirkhanian EA. Studies of the morphology of the
thyroid gland and thyroid hormone levels in the blood of
rats in experiments on Kosmos-1667 and Kosmos-1887.
Kosm Biol Aviakosm Med. 1990; 24:25-27.
53. Laugwitz K-L, Allgeier A, Offermanns S. The human
thyrotropin receptor: a heptahelical receptor capable of
stimulating members of all four G protein families. Proc
Natl Acad Sci. 1996; 93:116-120.
54. Van Sande J, Parma J, Tonacchera M, Swillens S,
Dumont J, Vassart G. Somatic and germline mutations of
the TSH receptor gene in thyroid diseases. J Clin
Endocrinol Metab. 1995; 80:2577-2585.
55. Dumont JE, Maenhaut C, Pirson I, Baptist M, Roger PP.
Growth factors controlling the thyroid gland. Baillieres
Clin Endocrinol Metab. 1991; 5:727-754.
56. Damante G, Dilauro R. Thyroid-specific gene expression.
Biochim Biophys Acta. 1994; 1218:255-266.
57. Steven I, Sherman MD, Jayashree Gopal MD, Bryan R,
Haugen MD, Alice C et al. Central Hypothyroidism
associated with retinoid x receptor–selective ligands N
Engl J Med. 1999; 340:1075-1079.
58. Peepre K, Bhimte B, Deshpandey U, Choudhary PS.
Antioxidants Protect Cell Damage from Free Radicals: A
research study on Thyroid Hormones in Wistar Rats.
59. IOSR Journal of Dental and Medical Sciences. 2014;
3(1):75-79.