Content uploaded by Jimmy Gutman
Author content
All content in this area was uploaded by Jimmy Gutman on Jun 22, 2017
Content may be subject to copyright.
Therapeutic Potential of Glutathione Augmentation in Cancer Patients
Receiving Chemotherapy or Radiotherapy
Jimmy Gutman*
Immunotec Research Inc. 300 Joseph Carrier, Vaudreuil-Dorion, Montreal, Canada
*Corresponding author: Jimmy Gutman, MD, Immunotec Research
Inc., 300 Joseph Carrier, Vaudreuil-Dorion, Montreal, Canada; Tel: +1
450 424 9992; Fax: +1 450 424 9993; E-mail: jgutman@immunotec.
com
Introduction
The search for selective injury or destruction to cancer
cells while limiting concomitant damage to normal cells has
been the cornerstone of cancer therapy. Surgical excision
is feasible if the tumor has not metastasized or a debulking
procedure is warranted.
Chemotherapy represents a controlled poisoning of the
patient based on the idea that rapidly proliferating cancer
cells are more sensitive to the toxin than normal cells. Un-
fortunately, many effective chemotherapeutic agents may
produce adverse side effects.
Radiotherapy works in a similar way. The cancerous
area is targeted for radioactive bombardment and the tumor
is theoretically more sensitive to the radiation than the sur-
rounding healthy tissues. This too carries potentially signi-
cant adverse effects for the patient.
Pretreatment or concomitant treatment with agents that
both enhance the selective toxicity of chemo/radiotherapy
to tumor cells while protecting healthy cells from damage
represents a welcome addition to standard approaches to
cancer therapy. The naturally-occurring tripeptide glutathi-
one (GSH) has been increasingly studied to play these roles.
GSH plays several critical roles in the normal physiolo-
gy of cells, including antioxidant regulation, detoxication,
protein synthesis and repair, immune modulation and redox
signaling [1]. Both increasing GSH levels and decreasing
GSH levels have been investigated in the search for effec-
tive glutathione modulatory approaches in oncology. This
present review article offers a synopsis of some historical
ndings.
Glutathione Modulation in Cancerous and Healthy Cells
Most studies reveal a paradoxical situation, where
cancer cells are high in glutathione [2], but normal cells
in cancer patients are low in glutathione compared to a
healthy population [3]. Notably, not only do low GSH lev-
els correlate with the susceptibility of individuals to develop
cancer [4, 5], but advanced cancer patients also reveal even
lower total body GSH levels [6]. More importantly, elevated
GSH in normal cells may offer increased protection from
the side effects of chemotherapy and radiotherapy and offer
an advantage in immune function and muscle preservation [7].
Experimental evidence shows that the level of GSH
synthesis affects the susceptibility of both normal and can-
cerous cells to damage from chemical toxins or radiation [8].
High GSH levels help protect cells from the harmful effects
of chemotherapy [9, 10]. Results would be ideal if GSH
levels were high in normal cells and low in tumorous cells
[11], but as stated, most human cancer cells appear to have
higher GSH levels than normal cells. Cancer is a rare ex-
ample where these otherwise tightly regulated GSH levels
are exceeded [12]. This is a consequence of lack of normal
GSH regulatory mechanisms in cancerous cells [8]. Be-
cause the tumor cells high in GSH often show resistance to
chemotherapy, some researchers have tried to reduce GSH
levels in cancerous cells with GSH-depleting drugs like
BSO (buthionine sulfoximine) [13]. A limiting consequence
of the use of BSO is its non-specic action, simultaneously
reducing GSH levels in healthy cells as well, resulting in the
magnication of side effects, thereby limiting the practicali-
ty of this approach [14].
Oddly enough, the precursors that usually raise GSH
levels in normal cells often cause the opposite effect in
cancerous cells, causing GSH levels to fall [15]. This is due
to a strong negative feedback loop in cancerous cells with
aberrant GSH production (Figure 1) [16]. These cells will
Abstract: The majority of cancer patients receiving conventional medical therapy receive chemotherapy,
radiotherapy, surgery or palliative support. Nutritional support is increasingly recognized as vital to successful
treatment. Glutathione (GSH) is a naturally-occurring tripeptide in human cells that serves many important functions,
including antioxidant regulation, detoxication, protein synthesis and repair, immune modulation, and redox signaling.
Altering glutathione levels has been demonstrated to have signicant effects in chemotherapy/radiotherapy outcomes as
well as inuence on retarding cachexia. This review article summarizes some of the most notable ndings, suggesting
that up-regulation of glutathione through nutritional intervention has a potential to be integrated into a holistic approach
to cancer treatment.
Key Words: Glutathione; Cancer; Chemotherapy; Radiotherapy; Cachexia; Nutrition; Immunocal
· 40 · Journal of Nutritional Oncology, November 15, 2016, Volume 1, Number 1
vanced progressive cancer, using toxic doses of acetamin-
ophen as the chemotherapeutic agent and rescuing patients
with NAC (n-acetyl-cysteine), which raises GSH levels.
Knowing that NAC selectively raises GSH levels in normal
cells, they were able to show either improvement or stabili-
zation in more than half the patients [19].
Additional studies have considered the effects of nu-
tritional proteins on cancer-causing chemicals in animals.
Researchers undertaking similar experiments in Canada and
Australia have subjected rodents to the powerful carcinogen
dimethylhydrazine—which causes colonic cancer—and fed
them with a variety of proteins [20, 21]. The animals fed
undenatured whey protein concentrate which raised GSH
levels, show fewer tumors and a reduced tumor load. The
scientists have found that this particular protein offered con-
siderable protection to the host.
Glutathione, Cancer, and Aging
It is accepted that the incidence and mortality rates of
cancer increase with age [22]. Certain cancers can in fact be
considered diseases of aging, most notably prostatic cancer
[23]. Specific changes in the aging individual’s immune
response and biochemical defenses such as antioxidant
function render them more susceptible to cancer [24]. The
protective effect of GSH diminishes with age. The aging
individuals may lose from 20 to 40% of GSH after age six-
ty-ve [25, 26]. This has been integrated into several theo-
ries of carcinogenesis in the elderly [27].
Studies show that normal levels of androgens in older
men lead to decreased GSH levels in prostatic tissue [28].
These androgens are known to act as oxidative stressors and
upset the prooxidant-antioxidant balance. This is believed to
be a possible mechanism by which prostatic carcinogenesis
develops.
Improved Tolerance to Chemo/Radiotherapy
Historically, the concurrent use of GSH augmentation
along with chemotherapy goes back several decades [29].
Gynecologic oncologists at the University of California
have treated patients with intravenous GSH along with the
standard chemotherapy cisplatin [30]. Higher doses of the
chemotherapy are possible, with fewer side effects.
A much larger study was performed at Western General
Hospital in Edinburgh, UK [31], in which over one hundred
and fifty patients with ovarian cancer were treated with
cisplatin along with intravenous GSH and were monitored
for side effects, quality of life, and outcome. They were
compared to equivalent patients not receiving GSH. The
group receiving the intravenous GSH showed a statistically
signicant improvement in depression, vomiting, hair loss,
shortness of breath, concentration, and neurotoxicity, and
the lab values measuring kidney function. There is a notable
trend toward improved outcome [31].
Alopecia (baldness) associated with chemotherapy cer-
tainly is not a life-threatening side-effect of chemotherapy,
down-regulate GSH production when intermediate steps
(e.g., glutamyl-cysteine) of GSH production are reached.
This negative feedback inhibition leaves cancerous tissue
more susceptible to damage or destruction while normal
cells, with normal GSH metabolism, are left with better de-
fense mechanisms [16].
Figure 1. Biochemical pathway of glutathione production
and regulation. Glutathione (gamma-glutamyl cysteine
glycine) inhibits its own production by down-regulating
gamma-glutamyl cysteine.
Clinical Trials
As far back as 1986, an NIH study demonstrated that
adding the GSH-promoting drug OTZ (2oxothia2oli-
dine-4-carboxylic acid) to human lung cancer cells, there
was no increase in GSH levels in the cancer cells, whereas
surrounding normal cells increased their levels [17]. Going
one step further, McGill University researchers Sylvain
Baruchel, Gerry Batist, and their team have demonstrated
that OTZ could even paradoxically deplete GSH content in
breast cancer cells while normal cells proted [11]. Another
study from McGill University led by Dr. Gustavo Bounous
has generated similar selective GSH modulatory results,
using whey protein isolates containing specic GSH precur-
sors [16].
Subsequently, studies have been performed on patients
with metastatic carcinoma, who were given this specially
prepared whey protein isolate for six months. Although it
did not cure the cancer, a significant proportion showed
either tumor regression/stabilization or normalization of
hemoglobin and white blood cell counts [18]. The same re-
searchers have demonstrated that elevated GSH levels may
enhance certain chemotherapeutic agents.
Another Canadian team has studied patients with ad-
Journal of Nutritional Oncology, November 15, 2016, Volume 1, Number 1 · 41 ·
but can be extremely distressing to the patient. It can also be
an indicator of the damage done to other high turnover cells
like those lining the intestine. Researcher Jimenez at the
University of Miami and others have demonstrated the abil-
ity of NAC to protect patients from the baldness resulting
from such common chemotherapy agents as cyclophospha-
mide [32].
Evidences exist suggesting that GSH-enhancing strat-
egies may improve the efficacy or tolerability of certain
chemotherapy agents, including adriamycin, cyclophospha-
mide, and cisplatin [7, 33-36]. However, a complete under-
standing of the mechanisms of chemoresistance to therapy
must be developed to suggest this strategy across the board
[37, 38].
Radiotherapists who have investigated the role of GSH
in protecting cells have been able to correlate higher pre-
treatment GSH levels with a lower amount of radiation
burns suffered afterwards [39]. Pre-treatment or simulta-
neous treatment with products to raise GSH, consistently
demonstrate a better tolerance to therapy [40].
Malnutrition/Wasting
Anti-cancer treatment is often accompanied by cachex-
ia, anorexia, fatigue, and decreased muscular strength. Good
nutrition is critical and often includes appropriate dietary
supplements [41]. The cancer itself, the anti-cancer treat-
ment and the resulting state of nutritional compromise all
decrease intracellular GSH levels [42]. This greatly weakens
antioxidant and immune defenses, rendering patients more
susceptible to other diseases and opportunistic infections
[43]. Wulf Droge has focused on cachexia in cancer, AIDS,
sepsis and other pathologies. He has noted the similarities
among them, pointing to a common cause—GSH and cyste-
ine depletion [44]. He and others have tested the possibility
that GSH-enhancing therapy may slow or halt this process
of degeneration [45].
Increased GSH synthesis depends on the intake of cyste-
ine-containing foods [16]. Rich sources of this GSH-precur-
sor are very hard to come by and often are not well tolerated
by the patient [46, 47]. Cysteine is available as a free amino
acid and may be ingested, but it has toxic qualities and does
not effectively raise GSH in humans [48]. The drugs NAC
and OTC can raise GSH levels but their effects are short-
lived [49]. These pharmaceutical drugs also have little
nutritional value. Whey proteins have excellent nutritional
value but usually lack biologically active GSH-precursors
[50]. The ideal source of dietary cysteine should be natural,
nutritional, bioactive, and undenatured [51]. The patented
whey protein Immunocal ts these criteria. It is biologically
active, sustains elevated GSH levels [52, 53], and has high
nutritional value.
In 2007 a multi-centered, double-blinded, placebo con-
trolled clinical trial was carried out in Canada [54]. The
objective of the study is to see if a specially-prepared whey
protein isolate (Immunocal) could improve quality-of-life
Conict of Interests
The author provides medical consultation to
Immunotec Research.
References
1. Aquilano K, Baldelli S, Ciriolo MR. Glutathione: new roles in
redox signaling for an old antioxidant. Front Pharmacol 2014;5:196.
2. Valko M, Leibfritz D, Moncol J, Cronin MT, Mazur M, Telser J.
Free radicals and antioxidants in normal physiological functions and
human disease. Int J Biochem Cell Biol 2007;39:44-84.
3. Franco R, Schoneveld OJ, Pappa A, Panayiotidis MI. The central
role of glutathione in the pathophysiology of human diseases. Arch
Physiol Biochem 2007;113:234-58.
4. Burlakova EB, Zhizhina GP, Gurevich SM, Fatkullina LD,
Kozachenko AI, Nagler LG, Zavarykina TM, Kashcheev VV.
Biomarkers of oxidative stress and smoking in cancer patients. J Cancer
Res Ther 2010;6:47-53.
5. Li XM, Yu XW, Yuan Y, Pu MZ, Zhang HX, Wang KJ, Han XD.
Glutathione S-transferase P1, gene-gene interaction, and lung cancer
susceptibility in the Chinese population: An updated meta-analysis and
review. J Cancer Res Ther 2015;11:565-70.
6. Karki K, Pande D, Negi R, Khanna S, Khanna RS, Khanna HD.
Association between biomarkers of oxidative stress, trace elements, and
cell proliferation index in patients with benign and malignant breast
diseases. J Environ Pathol Toxicol Oncol 2015;34:1-10.
7. Schmidinger M, Budinsky AC, Wenzel C, Piribauer M, Brix R,
variables in cancer patients receiving chemo/radiotherapy.
Outcomes show signicant improvement, and a statistically
signicant improvement in preventing and reversing weight
loss (cachexia) is evident. Additionally, an increase in sur-
vival is noted. This is an important evidence towards main-
taining that GSH augmentation is safe and effective when
combined with chemotherapy or radiotherapy.
Conclusion
Patients with higher intracellular GSH levels general-
ly demonstrate better prognosis and experience far fewer
chemotherapy side effects. In addition, the cells with higher
levels of GSH carry more protection against radiation dam-
age, thereby lessening the side effects of radiotherapy as
well. GSH modulation represents a novel approach to the
treatment and prevention of cancer. Moreover, the use of
GSH augmentation during chemotherapy or radiotherapy
shows promise as a complimentary treatment to improve
outcome and decrease side effects of therapy. Oral forms of
GSH do little to raise intracellular GSH levels. Intravenous
GSH has proven benets. Pharmacological GSH precursors
such as NAC have been demonstrated to be efcacious, but
provide no nutritive value. Specially prepared undenatured
whey protein isolate has the great advantage of delivering a
high biological value protein and at the same time serve as a
rich source of GSH precursors. This may offer the clinicians
an opportunity for dietary intervention that goes beyond just
nutritional support.
· 42 · Journal of Nutritional Oncology, November 15, 2016, Volume 1, Number 1
Kautzky M, Oder W, Locker GJ, Zielinski CC, Steger GG. Glutathione
in the prevention of cisplatin induced toxicities. A prospectively
randomized pilot trial in patients with head and neck cancer and non
small cell lung cancer. Wien Klin Wochenschr 2000;112:617-23.
8. Balendiran GK, Dabur R, Fraser D. The role of glutathione in
cancer. Cell Biochem Funct 2004;22:343-52.
9. Depeille P, Cuq P, Mary S, Passagne I, Evrard A, Cupissol D, Vian
L. Glutathione S-transferase M1 and multidrug resistance protein 1
act in synergy to protect melanoma cells from vincristine effects. Mol
Pharmacol 2004;65:897-905.
10. Traverso N, Ricciarelli R, Nitti M, Marengo B, Furfaro AL,
Pronzato MA, Marinari UM, Domenicotti C. Role of glutathione
in cancer progression and chemoresistance. Oxid Med Cell Longev
2013;2013:972913.
11. Baruchel S, Wang T, Farah R, Jamali M, Batist G. In vivo selective
modulation of tissue glutathione in a rat mammary carcinoma model.
Biochem Pharmacol 1995;50:1505-8.
12. Gamcsik MP, Kasibhatla MS, Teeter SD, Colvin OM. Glutathione
levels in human tumors. Biomarkers 2012;17:671-91.
13. Gallo JM, Brennan J, Hamilton TC, Halbherr T, Laub PB, Ozols
RF, O'Dwyer PJ. Time-dependent pharmacodynamic models in cancer
chemotherapy: population pharmacodynamic model for glutathione
depletion following modulation by buthionine sulfoximine (BSO) in a
Phase I trial of melphalan and BSO. Cancer Res 1995;55:4507-11.
14. Estrela JM, Ortega A, Obrador E. Glutathione in cancer biology
and therapy. Crit Rev Clin Lab Sci 2006;43:143-81.
15. Baruchel S, Viau G. In vitro selective modulation of cellular
glutathione by a humanized native milk protein isolate in normal cells
and rat mammary carcinoma model. Anticancer Res 1996;16:1095-9.
16. Bounous G. Whey protein concentrate (WPC) and glutathione
modulation in cancer treatment. Anticancer Res 2000;20:4785-92.
17. Russo A, DeGraff W, Friedman N, Mitchell JB. Selective
modulation of glutathione levels in human normal versus tumor cells
and subsequent differential response to chemotherapy drugs. Cancer
Res 1986;46:2845-8.
18. Kennedy RS, Konok GP, Bounous G, Baruchel S, Lee TD. The
use of a whey protein concentrate in the treatment of patients with
metastatic carcinoma: a phase I-II clinical study. Anticancer Res
1995;15:2643-9.
19. Kobrinsky NL, Harteld D, Horner H, Maksymiuk A, Minuk GY,
White DF, Feldstein TJ. Treatment of advanced malignancies with
high-dose acetaminophen and N-acetylcysteine rescue. Cancer Invest
1996;14:202-10.
20. Bounous G, Papenburg R, Kongshavn PA, Gold P, Fleiszer D.
Dietary whey protein inhibits the development of dimethylhydrazine
induced malignancy. Clin Invest Med 1988;11:213-7.
21. McIntosh GH, Regester GO, Le Leu RK, Royle PJ, Smithers GW.
Dairy proteins protect against dimethylhydrazine-induced intestinal
cancers in rats. J Nutr 1995;125:809-16.
22. Ames BN. Understanding the causes of aging and cancer.
Microbiologia 1995;11:305-8.
23. Miller KD, Siegel RL, Lin CC, Mariotto AB, Kramer JL, Rowland
JH, Stein KD, Alteri R, Jemal A. Cancer treatment and survivorship
statistics, 2016. CA Cancer J Clin 2016;66:271-89.
24. Richie JP Jr. The role of glutathione in aging and cancer. Exp
Gerontol 1992;27:615-26.
25. Julius M, Lang CA, Gleiberman L, Harburg E, DiFranceisco W,
Schork A. Glutathione and morbidity in a community-based sample of
elderly. J Clin Epidemiol 1994;47:1021-6.
26. Lang CA, Naryshkin S, Schneider DL, Mills BJ, Lindeman RD.
Low blood glutathione levels in healthy aging adults. J Lab Clin Med
1992;120:720-5.
27. Droge W. Aging-related changes in the thiol/disulfide redox
state: implications for the use of thiol antioxidants. Exp Gerontol
2002;37:1333-45.
28. Ripple MO, Henry WF, Rago RP, Wilding G. Prooxidant-
antioxidant shift induced by androgen treatment of human prostate
carcinoma cells. J Natl Cancer Inst 1997;89:40-8.
29. Plaxe S, Freddo J, Kim S, Kirmani S, McClay E, Christen R, Braly
P, Howell S. Phase I trial of cisplatin in combination with glutathione.
Gynecol Oncol 1994;55:82-6.
30. Gurtoo HL, Hipkens JH, Sharma SD. Role of glutathione
in the metabolism-dependent toxicity and chemotherapy of
cyclophosphamide. Cancer Res 1981;41:3584-91.
31. Smyth JF, Bowman A, Perren T, Wilkinson P, Prescott RJ, Quinn
KJ, Tedeschi M. Glutathione reduces the toxicity and improves quality
of life of women diagnosed with ovarian cancer treated with cisplatin:
results of a double-blind, randomised trial. Ann Oncol 1997;8:569-73.
32. Jimenez JJ, Huang HS, Yunis AA. Treatment with ImuVert/
N-acetylcysteine protects rats from cyclophosphamide/cytarabine-
induced alopecia. Cancer Invest 1992;10:271-6.
33. Cascinu S, Catalano V, Cordella L, Labianca R, Giordani P,
Baldelli AM, Beretta GD, Ubiali E, Catalano G. Neuroprotective effect
of reduced glutathione on oxaliplatin-based chemotherapy in advanced
colorectal cancer: a randomized, double-blind, placebo-controlled trial.
J Clin Oncol 2002;20:3478-83.
34. Block KI, Koch AC, Mead MN, Tothy PK, Newman RA,
Gyllenhaal C. Impact of antioxidant supplementation on
chemotherapeutic toxicity: a systematic review of the evidence from
randomized controlled trials. Int J Cancer 2008;123:1227-39.
35. Muldoon LL, Wu YJ, Pagel MA, Neuwelt EA. N-acetylcysteine
chemoprotection without decreased cisplatin antitumor efficacy in
pediatric tumor models. J Neurooncol 2015;121:433-40.
36. Prasad KN. Multiple dietary antioxidants enhance the efcacy of
standard and experimental cancer therapies and decrease their toxicity.
Integr Cancer Ther 2004;3:310-22.
37. Kwee JK. A paradoxical chemoresistance and tumor suppressive
role of antioxidant in solid cancer cells: a strange case of Dr. Jekyll and
Mr. Hyde. Biomed Res Int 2014;2014:209845.
38. Nakayama A, Alladin KP, Igbokwe O, White JD. Systematic
review: generating evidence-based guidelines on the concurrent use of
dietary antioxidants and chemotherapy or radiotherapy. Cancer Invest
2011;29:655-67.
39. Bhattathiri VN, Sreelekha TT, Sebastian P, Remani P, Chandini
R, Vijayakumar T, Nair MK. Inuence of plasma GSH level on acute
radiation mucositis of the oral cavity. Int J Radiat Oncol Biol Phys
1994;29:383-6.
40. De Maria D, Falchi AM, Venturino P. Adjuvant radiotherapy of
the pelvis with or without reduced glutathione: a randomized trial in
patients operated on for endometrial cancer. Tumori 1992;78:374-6.
Journal of Nutritional Oncology, November 15, 2016, Volume 1, Number 1 · 43 ·
41. Maschke J, Kruk U, Kastrati K, Kleeberg J, Buchholz D, Erickson
N, Huebner J. Nutritional care of cancer patients: a survey on patients'
needs and medical care in reality. Int J Clin Oncol 2017;22:200-6.
42. Kuyumcu A, Akyol A, Buyuktuncer Z, Ozmen MM, Besler HT.
Improved oxidative status in major abdominal surgery patients after
N-acetyl cystein supplementation. Nutr J 2015;14:4.
43. Droge W. Cysteine and glutathione in catabolic conditions
and immunological dysfunction. Curr Opin Clin Nutr Metab Care
1999;2:227-33.
44. Dröge W, Hack V, Breitkreutz R, Holm E, Shubinsky G, Schmid
E, Galter D. Role of cysteine and glutathione in signal transduction,
immunopathology and cachexia. Biofactors 1998;8:97-102.
45. Dröge W, Gross A, Hack V, Kinscherf R, Schykowski M,
Bockstette M, Mihm S, Galter D. Role of cysteine and glutathione
in HIV infection and cancer cachexia: therapeutic intervention with
N-acetylcysteine. Adv Pharmacol 1997;38:581-600.
46. Berk M, Dean OM, Cotton SM, Jeavons S, Tanious M, Kohlmann K,
Hewitt K, Moss K, Allwang C, Schapkaitz I, Robbins J, Cobb H, Ng F,
Dodd S, Bush AI, Malhi GS. The efcacy of adjunctive N-acetylcysteine in
major depressive disorder: a double-blind, randomized, placebo-controlled
trial. J Clin Psychiatry 2014;75:628-36.
47. Mallet P, Mourdi N, Dubus JC, Bavoux F, Boyer-Gervoise MJ,
Jean-Pastor MJ, Chalumeau M. Respiratory paradoxical adverse drug
reactions associated with acetylcysteine and carbocysteine systemic use
in paediatric patients: a national survey. PLoS One 2011;6:e22792.
48. Lomaestro BM, Malone M. Glutathione in health and disease:
pharmacotherapeutic issues. Ann Pharmacother 1995;29:1263-73.
49. Hamilton D, Batist G. Glutathione analogues in cancer treatment.
Curr Oncol Rep 2004;6:116-22.
50. Bounous G, Baruchel S, Falutz J, Gold P. Whey proteins as a
food supplement in HIV-seropositive individuals. Clin Invest Med
1993;16:204-9.
51. Bounous G, Gold P. The biological activity of undenatured dietary
whey proteins: role of glutathione. Clin Invest Med 1991;14:296-309.
52. PDR – Physicians Desk Reference, PDR Network, LLC, USA.
2016;70th Edition.
53. CPS – Compendium of Pharmaceuticals and Specialties, Canadian
Pharmacists Association, Canada 2016.
54. Tozer RG, Tai P, Falconer W, Ducruet T, Karabadjian A, Bounous
G, Molson JH, Dröge W. Cysteine-rich protein reverses weight loss in
lung cancer patients receiving chemotherapy or radiotherapy. Antioxid
Redox Signal 2008;10:395-402.
Received: September 19, 2016 Revised: October 4, 2016 Accepted: October 14, 2016
· 44 · Journal of Nutritional Oncology, November 15, 2016, Volume 1, Number 1
