Vol.3, No.8, 512-517 (2
Copyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
011) Health
Cortisol levels and serum antioxidant status following
Eugenia Limberaki1, Phaedra Eleftheriou1, Georgios Gasparis1, Eugenios Karalekos1, Vassilis
Kostoglou2*, Christos Petrou1
1Department of Medical Laboratory Studies, Alexander Technological Educational Institute of Thessaloniki, Thessaloniki, Greece;
2Department of Informatics, Alexander Technological Educational Institute of Thessaloniki, Thessaloniki, Greece;
*Corresponding Author: vkostogl@it.teithe.gr
Received 28 April 2011; revised 1 July 2011; accepted 13 July 2011.
Chemotherapy results in increased free radical
formation and depletion of tissue antioxidants.
Moreover, patients receiving chemotherapy are
under emotional stress, which is also accom-
panied by low antioxidant levels. In the present
study, we measured cortisol, the main stress
hormone, and total antioxidant capacity (TAC)
in serum of 51 cancer patients during chemo-
therapy. Antioxidant activity was estimated by
measuring the influence of serum in oxidation
of ABTS (2,2΄-azino-bis (3-ethylbenz-thiazoline-
6-sulfonic acid to ABTS+ by methmyoglobin
(Antioxidant kit of Cayman). Serum cortisol was
measured using an ELISA colorimetric assay.
Serum TAC was significantly decreased (75%
decrease compared to normal levels, p = 0.001)
in all patients during chemotherapy, while blood
cortisol concentration was increased by 10%, (p
= 0.044). Lower antioxidant levels and higher
cortisol concentration were detected in patients
receiving chemotherapeutic drugs daily, com-
pared to the ones receiving chemotherapy once
a week. A difference between sexes was ob-
served with male patients presenting lower an-
tioxidant status and higher cortisol levels than
females. A significant and persistent decrease
in antioxidant capacity accompanied by in-
creased cortisol concentration was observed in
all patients during chemotherapy. This fact,
which is probably generated by biological and
emotional stress, increases the probability of
harmful side effects and organism weakening
and needs to be considered during patients’
Keywords: Antioxidant Capacity; Cortisol;
Chemothera py; Cancer
Cancer cells themselves seem to cause a decrease in
antioxidant status [1]. Chemotherapy acts by killing cells
that divide rapidly, one of the main properties of most
cancer cells. Additionally, the action of most chemo-
therapeutic agents is based in creating reactive oxygen
species (ROS) [2,3], and these agents are associated with
depletion of plasma and tissue antioxidants [4-7]. ROS
are cytotoxic molecules and key mediators in signaling
cascades. Increased plasma lipid peroxidation and thio-
barbituric acid–reactive species accompany oxidative
stress induced in patients receiving chemotherapy [8,9].
Glutathione (GSH) concentrations are markedly reduced
by chemotherapeutic agents, such as busulfan, cermust-
ine (BCNU), and cisplatin [10]. Cisplatin is a platinum
containing anti-cancer drug reacting in vivo and causing
cross linking of DNA, which triggers to apoptosis. In ad-
dition, apoptosis induced by cisplatin is inhibited by
ROS scavengers, including N-acetyl cysteine, MnTBAP
and C60. Cisplatin promotes ROS production, which in
turn contributes to Fas receptor aggregation and cell
death. Newer anticancer drugs like nutlins act directly
against abnormal proteins in cancer cells; this is termed
target therapy and is technically not chemotherapy. The-
se drugs kill cancer cells via ROS-independent path-
ways. Phagocytosis of cancer cells may be another rea-
son for the generation of free radicals during chemo-
therapy [11]. The low serum total antioxidant capacity
observed in patients suffering from cancer reflects this
imbalance [12]. Insufficient defense against free radicals
may have harmful results, which may be the reason for
serious undesired side effects of chemotherapy. More-
over, it is hypothesized that ROS may facilitate metasta-
sis [13].
Many patients being treated for cancer receive dietary
supplements, particularly antioxidants, during chemothe-
rapy and radiotherapy [14,15]. Although some preclini-
E. Limberaki et al. / Health 3 (2011) 512- 517
Copyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
cal data show that antioxidants might reduce the effec-
tiveness of chemotherapy [16], other studies report
similar or better response in chemotherapy when com-
bined to antioxidant-rich diet [17-19]. For example,
while an excess in vitamin C is believed to facilitate glu-
cose transportation into cancer cells, thus inducing pro-
liferation [20-22], antioxidant vitamins such as C and E
have been successfully used as supplements for amelio-
rating the side effects of chemotherapy [23,24]. In gen-
eral, if generation of reactive oxygen species by a cancer
chemotherapeutic agent plays a role in its cytotoxicity,
antioxidants may interfere with the drug’s antineoplastic
activity. However, if the reactive species are responsible
only for the drug’s side effects, antioxidants may actu-
ally reduce the severity of such effects without interfer-
ing with the drug’s antineoplastic activity [2,25]. As a
consequence, different forms of antioxidant molecules
have been categorized either as interfering or not inter-
fering with anticancer therapy.
Cortisol, usually referred to as the “stress hormone”,
is involved in the organism’s response to stress and anxi-
ety. It triggers all metabolic mechanisms leading to pro-
duction of compounds used as energy sources in emer-
gency conditions. It increases glucose and free amino-
acid concentration in serum by inducing gluconeogene-
sis, thus inhibiting protein synthesis and promoting hy-
drolysis of lipids and proteins, and mobilization of extra
hepatic amino acids and ketone bodies. Cortisol levels
are affected by the circadian cycle with highest values
observed early in the morning. Increased cortisol con-
centrations are measured in blood serum of people under
biological or emotional stress, depression, sleep depriva-
tion, fever, hypoglycemia, anorexia nervosa and after
surgery [26-28]. A 3% - 10% increase in cortisol levels
has been observed in cancer patients varying according
to the severity of the disease [29]. Cortisol is one of the
main biomarkers of depression and is often used for
monitoring depression therapies [30]. Moreover, in-
crease in cortisol concentration has been associated with
decrease in total antioxidant levels and low total anti-
oxidant capacity (TAC) is a common feature in all con-
ditions where elevated cortisol concentrations are ob-
served [31]. The levels of some tissue antioxidants are
inversely related to cortisol tissue levels [32]. Antioxi-
dant depletion may result as a consequence of various
pathways activated by cortisol or may be the effect of
free radical production during cortisol metabolism, since
oxidative metabolism of cateholamines produces cinones
which react with superoxide anion, Ο2
, and hydrogen
dioxide, ΗΟ2
. Antidepressant therapy resulting in de-
crease of cortisol levels also results in increase of anti-
oxidant concentration. Moreover, it has been stated that
augmentation of antioxidant defense could serve as an
important mechanism underlying the neuroprotective
pharmacological effects of these drugs [33].
Cancer patients on chemotherapy are under strong
biological and emotional stress. This may lead to high
cortisol levels which may be an additional cause for the
reduction of protective antioxidants and induction of
undesired side effects.
In this study, we measured the total antioxidant capac-
ity and cortisol levels in serum of 51 cancer patients re-
ceiving chemotherapeutic agents once a day or once a
week and compared the concentrations of the two para-
meters between 1) patients and healthy people, 2) pa-
tients receiving the treatment once/day and once/week),
and 3) patients of different sex.
In the present study, the level of total blood antioxi-
dants and cortisol levels were measured in blood serum
of 51 (18 male and 33 female) Greek cancer patients on
chemotherapy. All blood samples were collected before
treatment between 8.00 and 9.00 a.m. All patients were
volunteers, informed about the project, and did not fol-
low any specific diet. The serum samples were stored for
3 - 15 days at –80˚C (Serum can be stored at –80˚C for 1
month as it is described in the Technical Bulletin of An-
tioxidant Assay Kit of Cayma). Lipemic and hemolysed
sampleswhen foundwere excluded. 19 of the pa-
tients received their chemotherapy agents once a day and
32 received their therapy once a week. Most chemo-
therapy agents consisted of busulfan, etoposide and
cyclopjosphamide, or cytosine, diaziquone and thiotepa.
For comparisons, samples from 32 men and women of
about the same age with no known health problem were
also collected and used as controls.
Evaluation of TAC was done using the antioxidant
Assay Kit of Cayman. Serum cortisol was measured
using the immunoenzyme assay kit of HUMAN. Ab-
sorbance rates were measured using START-FAX 2100
microtitre plate reader.
2.1. Evaluation of Serum Total Antioxidant
TAC measurement was carried out using the antioxi-
dant Assay Kit of Cayman. Antioxidants inhibit the oxi-
dation of ABTS (2.2΄-azino-di 3-ethylbenthiazoline-
sulfonate) to ABTS+ by methmyoglobin. Trolox, the
water soluble analogue of vitamin E, was used as control.
Antioxidant concentration is quantified in millimolar
Trolox equivalents [34].
2.2. Evaluation of Serum Cortisol
Serum cortisol was measured using the immunoen-
E. Limberaki et al. / Health 3 (2011) 512- 517
Copyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
zyme assay kit of HUMAN. The method is based on
competitive interaction of serum cortisol and a cortisol-
enzyme conjugated provided by HUMAN for a limited
number of monoclonal anti-cortisol antibodies bound to
the wells of a microtitre ELISA plate. The amount of the
bound hormone-enzyme conjugate is inversely propor-
tional to the concentration of cortisol in the specimen.
After removal of unbound conjugate by washing, a sub-
strate solution is added and a blue color develops which
changes to yellow by the addition of stop solution. The
absorbance is measured at 450 nm using a mictotitre
plate reader. Concentration of unknown specimens is
interpolated from a dose response curve generated by
utilizing serum calibrators of known cortisol concentra-
tion [35].
2.3. Statistical Analysis
Statistical analysis of data was carried out with SPSS
[36]. The Student’s t test for independent samples was
used to compare the blood samples of cancer patients
with them of healthy people. As this type of data follow
the normal distribution, we used the Student t-test to
detect significant differences between groups.
Measurement of the TAC in blood serum of 51 cancer
patients receiving chemotherapy and 32 healthy indi-
viduals of the same age revealed a 75% decrease in se-
rum antioxidants of treated cancer patients (p = 0.001
according to the Student’s t-test). Measurement of corti-
sol levels in the same blood samples revealed a 10%
increase in cortisol concentration in the patients’ group
(p = 0.044) (Figure 1).
TAC decrease was greater in patients receiving che-
motherapy once a day compared to the patients receiving
chemotherapy once a week (Figure 2).
Figure 1. Total antioxidant capacity and cortisol levels in
blood serum of cancer patients receiving chemotherapy (n = 51)
and healthy individuals (n = 32) of the same age (significance
levels according to the Student’s t-test: *p = 0.044, **p =
0.001). The vertical bars represent standard deviation (SD).
Figure 2. Total antioxidant capacity and cortisol levels in
blood serum of cancer patients receiving chemotherapy once a
day (n = 19) and once a week (n = 32) (significance levels
according to the Student’s t-test: *p = 0.101, **p = 0.001). The
vertical bars represent SD.
A statistically significant difference (p = 0.001) was
observed between the two groups of patients with total
blood antioxidant concentration in daily receiving che-
motherapy patients being 37% lower compared to the
weekly treated individuals. Greater elevation of cortisol
levels was measured in daily treated patients (D-T P)
compared to the weekly treated (W-T) ones. A 27% in-
crease in cortisol values of D-T P group was observed
compared to the W-T group (p = 0.101).
A difference both in TAC and cortisol levels of male
and female patients was also observed. Lower antioxi-
dant levels (21% decrease, p = 0.055) and higher cortisol
levels of poor significance though (29% increase, p =
0.214), were measured in male patients compared to the
female ones as shown in Figure 3.
Low antioxidant capacity was accompanied by high
cortisol levels in cancer patients on chemotherapy, al-
though some studies showed that cortisol can decrease
Figure 3. Total antioxidant capacity and cortisol levels in
blood serum of male (n = 18) and female (n = 33) cancer pa-
tients receiving chemotherapy (significance levels according to
the Student’s t-test:* p = 0.214, **p = 0.055). The vertical bars
represent SD.
E. Limberaki et al. / Health 3 (2011) 512- 517
Copyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
oxidative stress through inhibition of nuclear factor-κB
[37,38] The decrease in antioxidant capacity reached
72% in weekly treated patients and 82% in daily treated
patients compared to the control group. Since, most of
the chemotherapeutic agents are cleared-off within hours
or a few days, this means that a slight part of the de-
crease observed was due to the presence of the chemo-
therapeutic agent itself and low TAC was observed at
least seven days after application of chemotherapy. This
was a common finding in all patients and was not de-
pendent on the chemotherapeutic agent used. A 10% -
20% decrease in TAC is a common characteristic in pa-
tients suffering from cancer and was observed in benign
and malignant neoplasias [39]. Emotional and biological
stress and cytotoxic procedures may also contribute to
that decrease. Increased cortisol concentrations were
measured in all patients. A 10% average increase was
observed in weekly-treated patients reaching 64% in-
crease in daily-treated patients. Although, a straight rela-
tionship between antioxidant status and cortisol levels
was not obtained from our results, high cortisol concen-
tration may partly contribute to TAC decrease especially
in daily-treated patients.
Exposure to stressful conditions often leads to high
cortisol levels, smoothening at the same time, the dif-
ferences existing because of sex or age [40]. Some pub-
lished studies showed a significant reduction in serum
cortisol immediately after infusion of either cisplatin or
carboplatin and other chemotherapeutic agent like ly-
sodren which works by attacking the cells of the adrenal
glands to inhibit adrenal gland functioning [41].
However, this was not observed in the present study. It
seems that additional excretion of the hormone due to
chemotherapy is added to the already elevated levels in
male patients [42] or that male patients respond in a dif-
ferent way in stressful conditions. Different response to
chemotherapy is also reflected in the antioxidant levels
in serum of the two sexes. Sex differences in symptoms
and response to a therapy has often been observed in
cancer patients [43].
In spite of the suggestion of some researchers that
treatment with antioxidants may reduce the effect of
some anticancer agents, we believe that such a great and
persistent decrease in antioxidant capacity accompany-
ing increased cortisol concentrations augments the prob-
ability of harmful side-effects and may lead to the orga-
nism weakening. We conclude that, depending on the
treatments used against cancer, a special diet or treat-
ment aiming at the improvement of patients’ antioxidant
capacity and reduction of cortisol concentration may
upgrade the health status of patients and their response
to therapies in general.
The authors thank Dr Yannis Kazoglou for useful comments on the
[1] Skrzydlewska, E., Stankiewicz, A., Sulkowska, M., Sul-
kowski, S. and Kasacka, I. (2001) Aantioxidant status
and lipid peroxidation in colorectal cancer. Journal of
Toxicolog y and E n v ironmental Health, 64, 213-222.
[2] Shacter, E., Williams, J.A., Hinson, R.M., Senturker, S.
and Lee, Y.J. (2000) Oxidative stress interferes with can-
cer chemotherapy: Inhibition of lymphoma cell apoptosis
and phagocytosis. Blood, 96, 307-313.
[3] Lee, Y.J. and Shacter, E. (1999) Oxidative stress inhibits
apoptosis in human lymphoma cells. Journal of Biolo-
gical Chemistry, 274, 19792-19798.
[4] Weijl, N.I., Leton, F.J. and Osanto, S. (1997) Free radi-
cals and antioxidants in chemotherapy-induced toxicity.
Cancer Tr eatment Reviews, 23, 209-240.
[5] Durken, M., Agbenu, J., Finckh, B., Hübner, C., Pichl-
meier, U., Zeller, W., et al. (1995) Deteriorating free
radicaltrapping capacity and antioxidant status in plasma
during bone marrow transplantation. Bone Marrow
Transplant, 15, 757-762.
[6] Lauterburg, B.H., Nguyen, T., Hartmann, B., Junker, E.,
Kupfer, A. and Cerny, T. (1994) Depletion of total cys-
teine, glutathione, and homocysteine in plasma by ifos-
famide/mesna therapy. Cancer Chemotherapy and
Pharmacology, 35,132-136. doi:10.1007/BF00686635
[7] Crohns, M., Liippo, K., Erhola, M., Kankaanranta, H.,
Moilanen, E., Alho, H., et al. (2009) Concurrent decline
of several antioxidants and markers of oxidative stress
during combination chemotherapy for small cell lung
cancer. Clinical Biochemistry, 42, 1236-1245.
[8] Ladner, C., Ehninger, G., Gey, K.F. and Clemens, M.R.
(1989) Effect of etoposide (VP16–213) on lipid peroxi-
dation and antioxidant status in a highdose radiochemo-
therapy regimen. Cancer Chemotherapy and Pharma-
cology, 25, 210-212. doi:10.1007/BF00689585
[9] Faure, H., Coudray, C., Mousseau, M., Ducros, V., Douki,
T., Bianchini, F., et al. (1996) 5-Hydroxymethyluracil
excretion, plasma TBARS and plasma antioxidant vita-
mins in adriamycin-treated patients. Free Radical Biol-
ogy and Medicine, 20, 979-983.
[10] Bhuvarahamurthy, V., Balasubramanian, N. and Govin-
dasamy, S. (1996) Effect of radiotherapy and chemo-
therapy on circulating antioxidant system of human uter-
ine cervical carcinoma. Molecular and Cellular Bio-
chemistry, 158, 17-23.
[11] Gadjeva, V., Dimov, A. and Georgieva, N. (2008) Influ-
ence of therapy on the antioxidant status in patients with
melanoma. Journal of Clinical Pharmacy and Therapeu-
tics, 33, 179-185. doi:10.1111/j.1365-2710.2008.00909.x
[12] Papageorgiou, M., Stiakaki, E., Dimitriou, H., Malliaraki,
N., Notas, G., Castanas, E., et al. (2005) Cancer chemo-
therapy reduces plasma total antioxidant capacity in
children with malignancies. Leukemia Research, 29, 11-
E. Limberaki et al. / Health 3 (2011) 512- 517
Copyright © 2011 SciRes. Openly accessible at http://www.scirp.org/journal/HEALTH/
16. doi:10.1016/j.leukres.2004.04.017
[13] Ten Kate, M., van der Wal, J.B., Sluiter, W., Hofland, L.J.,
Jeekel, J., Sonneveld, P., et al. (2008) The role of super-
oxide anions in the development of distant tumour recur-
rence. British Journal of Cancer, 98, 580-586.
[14] Burstein, H.J., Gelber, S., Guadagnoli, E. and Weeks, J.C.
(1999) Use of alternative medicine by women with
early-stage breast cancer. New England Journal of Medi-
cine, 340, 1733-1739.
[15] Van de Creek, L., Rogers, E. and Lester, J. (1999) Use of
alternative therapies among breast cancer outpatients
compared with the general population. Alternative Thera-
pies in Health and Medicine, 5, 71-76.
[16] D’Andrea, G.M. (2005) Use of antioxidants during che-
motherapy and radiotherapy should be avoided. A Cancer
Journal for Clinicians, 55, 319-321.
[17] Pace, A., Savarese, A., Picardo, M., Maresca, V., Pacetti,
U., Del Monte, G., et al. (2003) Neuroprotective effect of
vitamin E supplementation in patients treated with cis-
platin chemotherapy. Journal of Clinical Oncology, 21,
927-931. doi:10.1200/JCO.2003.05.139
[18] Iarussi, D., Auricchio, U., Agretto, A., Murano, A.,
Giuliano, M., Casale, F., et al. (1994) Protective effect of
coenzyme Q10 on anthracyclines cardiotoxicity: Control
study in children with acute lymphoblastic leukemia and
non-Hodgkin lymphoma. Molecular Aspects of Medicine,
15, 207-212.
[19] Weijl, N.I., Elsendoorn, T.J., Lentjes, E.G., Hopman, G.D.,
Wipkink-Bakker, A., Zwinderman, A.H., et al. (2004)
Supplementation with antioxidant micronutrients and
chemotherapy-induced toxicity in cancer patients treated
with cisplatin-based chemotherapy: A randomised, dou-
ble-blind, placebo-controlled study. European Journal of
Cancer, 40, 1713-1723.
[20] Guaiquil, V.H., Vera, J.C. and Golde, DW. (2001) Mecha-
nism of vitamin C inhibition of cell death induced by
oxidative stress in glutathione-depleted HL-60 cells. Jour-
nal of Biological Chemistry, 276, 40955-40961.
[21] Lesperance, M.L., Olivotto, I.A., Forde, N., Zhao, Y.,
Speers, C., Foster, H., et al. (2002) Mega-dose vitamins
and minerals in the treatment of non-metastatic breast
cancer: An historical cohort study. Breast Cancer Re-
search and Treatment, 76, 137-143.
[22] Bjelakovic, G., Nikolova, D., Simonetti, R.G. and Gluud,
C. (2004) Antioxidant supplements for prevention of
gastrointestinal cancers: A systematic review and meta-
analysis. Lancet , 364, 1219-1228.
[23] Greggi Antunes, L.M., Darin, J.D. and Bianchi, M.D.
(2000) Protective effects of vitamin C against cisplatin-
induced nephrotoxicity and lipid peroxidation in adult
rats: A dose-dependent study. Pharmacological Research,
41, 405-411. doi:10.1006/phrs.1999.0600
[24] Chinery, R., Brockman, J.A., Peeler, M.O., Shyr, Y.,
Beauchamp, R.D. and Coffey, R.J. (1997) Antioxidants
enhance the cytotoxicity of chemotherapeutic agents in
colorectal cancer: A p53-independent induction of p21
WAF1/CIP1 via C/EBPbeta. Nature Medicine, 3, 1233-
[25] Daubeuf, S., Balin, D., Leroy, P. and Visvikis, A. (2003)
Different mechanisms for gamma-glutamyltranspepti-
dase-dependent resistance to carboplatin and cisplatin.
Biochemical Pharmacology, 66, 595-604.
[26] Agelaki, S., Tsatsanis, C., Gravanis, A. and Margioris,
A.N. (2002) Corticotropin-releasing hormone augments
proinflammatory cytokine production from macrophages
in vitro and in lipopolysaccharide-induced endotoxin
shock in. Infection and Immunity, 70, 6068-6074.
[27] Lovallo, W.R., Farag, N.H., Vincent, A.S., Thomas, T.L.
and Wilson, M.F. (2006) Cortisol responses to mental
stress, exercise, and meals following caffeine intake in
men and women. Pharmacology Biochemistry and Be-
haviour, 83, 441-447. doi:10.1016/j.pbb.2006.03.005
[28] Ruzic, B., Tomaskovic, I., Trnski, D., Kraus, O., Beka-
vac-Beslin, M. and Vrkic, N. (2005) Systemic stress re-
sponses in patients undergoing surgery for benign pro-
static hyperplasia. BJU International, 95, 77-80.
[29] Lutgendorf, SK., Weinrib, A.Z., Penedo, F., Russell, D.,
DeGeest, K. and Costanzo, E. (2008) Interleukin-6, cor-
tisol, and depressive symptoms in ovarian cancer patients.
Journal of Clinical Oncology, 26, 4820-4827.
[30] Young, A.H. (2004) Cortisol in mood disorders. St ress, 7,
[31] Wang, L., Muxin, G., Nishida, H., Shirakawa, C., Sato, S.
and Konishi, T. (2007) Psychological stress-induced oxi-
dative stress as a model of sub-healthy condition and the
effect of TCM. Evidence Based Complementary and Al-
ternative Medicine, 4, 195-202.
[32] Marusin, A.V., Salyukov, V.B. and Yu Bragina, E. (2002)
Antioxidant activity of blood plasma in individuals with
neoplasms. Bulletin of Experimental Biology and Medi-
cine, 133, 481-483.
[33] Thakor, A.S. and Giussani, D.A. (2005) Antioxidants
enhance the adrenocortical response to stress in the fetus.
Endocrine Abstracts, 196th Meeting of the Society for
Endocrinology, London, UK, 7-9 November 2005, 10
[34] Erel, O.A. (2004) Novel automated method to measure
total antioxidant response against potent free radical re-
actions. Clinical Biochemistry, 37, 112-119.
[35] Perry, L.A. and Gossman, A.B. (1997) The role of the
laboratory in the diagnosis of Cushing’s syndrome. An-
nals of Clinical Biochemistry, 34, 345-359.
[36] Press, W.H., Teukolsky, S.A., Vetterling, W.T. and Flan-
nery B.P. (1992) Numerical Recipes in C: The art of sci-
entific computing. Cambridge University Press, Cam-
[37] Almawi, W.Y. and Melemedjian, O.K. (2002) Negative
regulation of nuclear factor-kappab activation and func-
tion by glucocorticoids. Journal of Molecular Endocri-
nology, 28, 69-78. doi:10.1677/jme.0.0280069
[38] Marumo, T., Schini-Kerth, V.B., Brandes, R.P. and Busse,
R. (1998) Glucocorticoids inhibit superoxide anion pro-
duction and p22 phox mRNA expression in human aortic
smooth muscle cells. Hypertension, 32, 1083-1088.
[39] Pejić, S., Todorović, A., Stojiljković, V., Cvetković, D.,
Lucić, N., Radojicić, R.M., et al. (2008) Superoxide
dismutase and lipid hydroperoxides in blood and endo-
metrial tissue of patients with benign, hyperplastic and
malignant endometrium. Annals of the Brazilian Acad-
emy of Science, 80, 515-522.
E. Limberaki et al. / Health 3 (2011) 512- 517
Copyright © 2011 SciRes. http://www.scirp.org/journal/HEALTH/ Openly accessible at
[40] Swaab, D.F., Raadsheer, F.C., Endert, E., Hofman Kam-
phorst, M.W. and Ravid, R. (2006) Increased cortisol
levels in Aging and Alzheimer’s disease in postmortem
cerebrospinal fluid. Journal of Neuroendocrinology, 6,
681-687. doi:10.1111/j.1365-2826.1994.tb00635.x
[41] Morrow, G.R., Hickok, J.T., Andrews, P.L. and Stern,
R.M. (2002) Reduction in serum cortisol after platinum
based chemotherapy for cancer: A role for the HPA axis
in treatment-related nausea? Psychophysiology, 39, 491-
495. doi:10.1111/1469-8986.3940491
[42] Paris, J.J., Franco, C., Sodano, R., Freidenberg, B.,
Gordis, E., Anderson, D.A., et al. (2010) Sex differences
in salivary cortisol in response to acute stressors among
healthy participants, in recreational or pathological gam-
blers, and in those with posttraumatic stress disorder.
Hormones and Behaviour, 57, 35-45.
[43] McCann, J. (2000) Gender differences in cancer that
don’t make sense—Or do they? Journal of the National
Cancer Institute, 92, 1560-1562.