PHYTOTHERAPY RESEARCH

Phytother. Res. 17, 1076–1081 (2003)

1076 Published online in Wiley InterScience (www.interscience.wiley.com).
M. FRANCO-MOLINA ET DOI:
AL.10.1002/ptr.1313

In vitro Immunopotentiating Properties and

Tumour Cell Toxicity Induced by Lophophora
williamsii (Peyote) Cactus Methanolic Extract

M. Franco-Molina, R. Gomez-Flores, P. Tamez-Guerra, R. Tamez-Guerra, L. Castillo-Leon

and C. Rodríguez-Padilla*
Departamento de Microbiología e Inmunología, Facultad de Ciencias Biológicas, Universidad Autónoma de Nuevo León, San
Nicolás de los Garza, NL, México

Lophophora williamsii, also known as peyote, is found primarily in dry regions from Central Mexico, includ-
ing the Mexican States of Nayarit, San Luis Potosí, Zacatecas, Nuevo León, Chihuahua, Coahuila and
Tamaulipas, to Texas particularly in regions along Rio Grande. Peyote extracts have been associated with
stimulating the central nervous system and regulating blood pressure, sleep, hunger and thirst. However, there
is no evidence of any effect of peyote on the immune system or against tumour cell growth. The present study
was designed to evaluate the in vitro effects of peyote methanolic extracts on some parameters of mouse and
human leukocyte immunocompetence and tumour cell growth. Peyote extract (0.18–18 µg/mL) activated nitric
oxide production by murine macrophages, and stimulated up to 2.4-fold proliferation of murine thymic
lymphocytes. In addition, peyote extract induced up to 1.85-, 2.29- and 1.89-fold increases in mRNA signal of
IL-1, IL-6 and IL-8 by human leukocytes. Also examined were the effects of peyote extracts on murine
lymphoma L5178Y-R and fibroblastoma L929, and human myeloid U937 and mammary gland MCF7 tumour
cell growth using 3-[4,5-dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide (MTT). Peyote extracts were
toxic for MCF7, L5178Y-R, U937 and L929 (18 µg/mL peyote extract caused 1.3%, 8%, 45% and 60%
viability respectively) cell lines. Copyright © 2003 John Wiley & Sons, Ltd.

Keywords: Lophophora williamsii; peyote extract; methanol extract; in vitro; immunopotentiation; antitumour activity.

Regardless of a number of studies reporting that

INTRODUCTION
Lophophora williamsii also known as peyote, devil’s
root, dumpling cactus, mescal button, and sacred
mushroom, is a 2–5 inches in diameter spineless, tufted,
blue-green, button-like cactus. It grows wild from
Central Mexico, including the mexican States of Nayarit,
Querétaro, San Luis Potosí, Durango, Zacatecas, Nuevo
León, Baja California Norte, Chihuahua, Coahuila,
Tamaulipas and Sonora, to Texas along Rio Grande
from Presidio County to Starr and Jim Hogg Counties,
and is commonly used by Arapaho, Blackfoot, Com-
anche, Huichol, Kickapoo, Kiowa, Lakota, Navajo,
Omaha, Winnebago Indian Tribes (McLaughlin, 1973;
Borchers et al., 2000). Peyote is a hallucinogen cactus
associated with producing significant physical, visual, and
perceptual changes (Hermle et al., 1992). In addition, it
is used to treat infections, arthritis, asthma, influenza,
intestinal disorders, diabetes, snake and scorpion bites.
L. williamsii is considered illegal in the United States,
except for members of the Native American Church.
cancer incidence rates among Native Americans
are significantly lower than the general population
(Michalek and Mahoney, 1990), there is no evidence of
peyote action on the immune system or against tumor
cell growth. Interestingly, others have hypothesized
that by stimulating mystical experiences, entheogens/
psychedelic drugs can boost the immune system and
promote cancer remission (Roberts, 1999). Then, it is
plausible to consider that hallucinogenic/psychedelic
substances may alter the state of mind of individuals in
such a way that it can positively influence their health
status. In this regard, it is recognized that religion could
impact physical health through neuroendocrine and
immune mechanisms (Koenig, 2000).
The present study was designed to evaluate the
effects of the methanol extract of L. williamsii on some
in vitro parameters of immune function of murine
lymphocytes and macrophages, and human peripheral
blood mononuclear cells (HPBMC), and on murine and
human tumour cell growth.

* Correspondence to: Dr C. Rodríguez-Padilla, Departamento de

MATERIAL AND METHODS
Microbiología e Inmunología, Facultad de Ciencias Biológicas, Universidad
Autónoma de Nuevo León, Loma Larga 2302, Colonia Obispado,
Monterrey, NL, México CP64060. Reagents, culture media and cell lines. Penicillin-
E-mail: crrodrig@ccr.dsi.uanl.mx streptomycin solution, l-glutamine, ficoll-hypaque
Contract/grant sponsor: Consejo Nacional de Ciencia y Tecnología;
contract/grant number: I-32914-N.
solution, trypsin-EDTA solution, and RPMI 1640
Contract/grant sponsor: Universidad Autónoma de Nuevo León, México; and AIM-V media were obtained from Life Techno-
contract/grant number: CN-285-00. logies (Grand Island, NY). Fetal bovine serum (FBS),
Copyright © 2003 John Wiley & Sons, Ltd. Received
Phytother. Res. 5 February(2003)
17, 1076–1081 2002
Accepted 3 February 2003
Copyright © 2003 John Wiley & Sons, Ltd.
 IMMUNOPOTENTIATION BY LOPHOPHORA WILLIAMSII EXTRACT
lipopolysaccharide (LPS) from Escherichia coli
serotype 026:B6, sodium dodecyl sulfate (SDS),
N,N-dimethylformamide (DMF), PBS and 3-[4,5-
dimethylthiazol-2-yl]-2,5-diphenyltetrazolium bromide
(MTT) were purchased from Sigma Chemical Co.
(St Louis, MO). The murine fibrosarcoma L929 (clone
CCL 1), murine lymphoma L5178Y-R (clone CRL-
1722), human histiocytic lymphoma (U937, clone CRL
1593) and human breast cancer MCF7 (clone HTB-22)
cell lines were purchased from the American Type
Culture Collection (Rockville, MD). Tumour cell lines
were maintained in RPMI 1640 medium supplemented
with 10% FBS, 1% l-glutamine, and 0.5% penicillin-
streptomycin solution (referred to as complete RPMI
1640 medium). Extraction buffer was prepared by
dissolving 20% (w/v) SDS at 37 °C in a solution of
50% each DMF and demineralized water, and the pH
was adjusted to 4.7.
Preparation of Lophophora williamsii extract. The
cactus material used in this study was identified as
Lophophora williamsii (Lem.) Coult., commonly known
as ‘peyote’, by M.Sci. María del Consuelo González de
la Rosa, Chief of the Herbarium of the Biological
Sciences College at Autonomous University of Nuevo
Leon, with a voucher specimen 008877 (UAN). Peyote
was collected on a hill in a wild and dry area of Villa
de García, Nuevo León, located northeast of México.
Peyote’s tubercle (50 g) was macerated in a blender,
treated with 50 mL of methanol for 48 h at 4 °C, and
the extract was filtered. Two-ml aliquots of the meth-
anol extract were then frozen with a dry-ice acetone
mixture, and lyophilized for 2 days by using a freeze-
dryer (Labconco Co., Kansas City, MO). The resulting
powder (76 mg) was dissolved in 1 mL of complete
RPMI 1640 medium. Experimental concentrations were
prepared from this stock solution and dilutions were
made in complete RPMI 1640 medium. Endotoxin
levels in peyote extract were negligible (a maximum
of 12 ng of endotoxin in 18 µg/mL of the extract) at a
detection limit of 0.004 ng/mL in the gel clot-based
Limulus amoebocyte assay (Associates of Cape Cod,
Falmouth, MA).
Animals. Six-week-old female BALB/c mice (22–28 g)
were purchased from Harlan Sprague-Dawley Inc.
(Indianapolis, IN). They were kept in a pathogen- and
stress-free environment at 24 °C, under a light–dark
cycle (light phase, 06:00–18:00 h), and given water and
food ad libitum.
Cell preparation and culture. Thymus was immedia-
tely removed after mouse death. Single-cell suspen-
sions were prepared by disrupting the thymus in RPMI
1640 medium. Cell suspensions were then washed three
times in this medium, and suspended and adjusted to
1 × 107 cells/mL with AIM-V medium (containing 0.5%
penicillin-streptomycin solution). The culture medium
was changed at this step to the serum-free medium
AIM-V which has been observed to support cell cul-
ture (Kaldjian et al., 1992). Peritoneal macrophages
were prepared by washing the peritoneal cavity with
cold RPMI 1640 medium, and washing the resulting
cell suspension twice in this medium. One hundred-
microlitre cell suspensions at 1.7 × 106 cells/mL in
AIM-V medium were then plated in flat-bottomed
Copyright © 2003 John Wiley & Sons, Ltd.
1077
96-well plates (Becton Dickinson) for 2 h at 37 °C.
Non-adherent cells were removed, and adherent cells
(about 70% of the input cells or about 1 × 106 cells/mL)
were then utilized for determining nitric oxide produc-
tion. The final adherent cell monolayer consisted of
95%–99% macrophages as judged by Giemsa’s stain
procedures.
T cell proliferation assay. T cell proliferation was
determined by a colorimetric technique using MTT
(Hansen et al., 1989). Thymic cell suspensions (100 µL)
were added to flat-bottomed 96-well plates (Becton
Dickinson) containing triplicate cultures (100 µL) of
AIM-V medium (unstimulated control) or peyote
extract at various concentrations. After incubation
for 44 h at 37 °C with 5% CO2, MTT (0.5 mg/mL, final
concentration) was added, and cultures were addi-
tionally incubated for 4 h. Cell cultures were then
incubated for 16 h with extraction buffer (100 µL) and
optical densities, resulting from dissolved formazan
crystals, were then read in a microplate reader (Bio-
Tek Instruments, Inc., Winooski, VT) at 540 nm.
Nitrite determination. Accumulation of nitrite in the
supernatants of macrophage cultures was used as an
indicator of nitric oxide production by resident or
activated cells. Peritoneal macrophages were incubated
for 72 h in 200 µL AIM-V medium, in the presence
or absence of various concentrations of peyote extract
or LPS (10 and 20 µg/mL) in triplicate, in a total
volume of 200 µL AIM-V medium. After incubation,
supernatants were obtained and nitrite levels were
determined with the Griess reagent (Gomez-Flores
et al., 1997), using NaNO2 as standard. Optical densities
at 540 nm were then determined in a microplate reader
(Bio-Tek Instruments, Inc.). Macrophage viability was
determined by the MTT reduction assay as previously
described (Hansen et al., 1989).
The percentage of viability was calculated as follows:
A540 in peyote extract-treated cells
% viability = × 100
A540 in untreated cells
Effect of peyote extract on HPBMC. Leukocytes were
obtained from peripheral blood of healthy volunteers,
and centrifuged in a 1.077 g/dL ficoll-hypaque solution
for 30 min at 10 °C and 1600 rpm. The recovered
mononuclear cells were washed twice in RPMI 1640
medium, and adjusted to 5 × 106 cells/mL in complete
RPMI 1640 medium. One hundred microlitres of the
leukocyte suspension was then incubated for 72 h in
the presence or absence of various concentrations (0.18–
18 µg/mL) of peyote extract in a volume of 100 µL.
After incubation for 68 h at 37 °C in 5% CO2, 20 µL of
MTT (0.5 mg/mL final concentration) was added to
all wells, and cultures were incubated for an addi-
tional 4 h. After this, extraction buffer was added to
all wells and plates were incubated for 16 h. Optical
densities were then measured by absorption at 540 nm
as described above. For inflammatory cytokine gene
expression, whole HPBMC was incubated with various
concentrations of peyote extract for 5 h at 37 °C, 95%
CO2–5% air, after which mononuclear cells were ob-
tained by centrifugation on a ficoll-hypaque gradient.
The recovered mononuclear cells were washed twice in
RPMI 1640 medium, and adjusted to 5 × 106 cells/mL
Phytother. Res. 17, 1076–1081 (2003)
1078 M. FRANCO-MOLINA ET AL.

in AIM-V medium. Next, trizol was added to the cells

to extract total RNA. Gene expression for inflamma-
tory cytokines was then detected by RT-PCR as re-
ported elsewhere (Hernandez-Pando et al., 1996).

Effect of peyote extract on murine and human tumour

cell growth. Exponentially growing tumour cell lines
were plated at 1 × 106 cells/mL (L5178Y-R and U937),
1 × 105 cells/mL (L929) and 5 × 104 cells/mL (MCF7)
in flat-bottomed 96-well plates (Becton Dickinson,
Lincoln Park, NJ) in 100 µL of complete RPMI 1640
medium. These tumour cell cultures were then incu-
bated for 72 h in the presence or absence of various
concentrations (0.18–18 µg/mL) of peyote extract in a
volume of 100 µL. After incubation for 68 h at 37 °C
in 5% CO2, 10 µL of MTT (0.5 mg/mL final concentra-
tion) was added to all wells, and cultures were addi-
tionally incubated for 4 h. After this, 100 µL extraction
buffer was added to all wells and plates were incubated
for 16 h. Optical densities and percent viability were
then determined by absorption at 540 nm as described
above.
Figure 1. Lymphoproliferation induced by L. williamsii extract
Statistical analysis. The results were expressed as mean and concanavalin A. Murine thymic cell suspensions were
incubated in the presence or absence of various concentra-
± SD of triplicate determinations from a representative tions of peyote extract (a) or concanavalin A (b), after which
experiment. All experiments were repeated at least lymphoproliferation was measured by a colorimetric technique,
three times with similar results. Statistical significance as explained in the text. Data represent means of triplicate
was assessed by one-way analysis of variance. determinations from a representative experiment (standard
deviations were less than 1% of the means). Proliferation
index = A540 of treated cells/A540 of untreated cells. ** p < 0.01,
* p < 0.05 compared with untreated control. Optical density value
for thymic lymphocyte proliferation in medium alone (untreated
RESULTS control) was 0.122 ± 0.003.

Lymphoproliferation induced by L. williamsii extract

As observed in Fig. 1a, L. willamsii extract at all con-

centrations tested, induced 1.5- to 2.4-fold significant
(p < 0.05) increases in the proliferation of murine thymic
lymphocytes. By comparison, lymphocyte proliferation
indexes to concanavalin A at concentrations of 0.6,
1.2 and 2.4 µg/mL were 2.6, 3.6 and 1.5, respectively
(Fig. 1b).

Nitric oxide production induced by L. williamsii

extract
Nitrite levels in supernatants of murine macrophage
cultures treated with L. williamsii extract (between
5.4 µg/mL and 18 µg/mL) were significantly (p < 0.05)
higher than those of the untreated control (negligible
nitrite levels) (Fig. 2). By comparison, nitrite levels
induced by LPS at concentrations of 10 and 20 µg/mL
were 2.02 ± 0.31 and 3.35 ± 0.19 nmol/well, respectively
(data not shown). In addition, a 0.7% to 35% reduc-
tion of viability of murine macrophages treated with
L. williamsii extract at concentrations ranging from 5.4
to 18 µg/mL respectively (correlation coeficient 0.95),
was observed (Fig. 2).
Effect of L. williamsii extract on inflammatory
cytokine gene expression and viability of HPBMC
In addition to measuring the effects of L. williamsii
extract on some parameters of immune function in
Copyright © 2003 John Wiley & Sons, Ltd.
Figure 2. Effect of L. williamsii extract on the production
of nitric oxide by murine macrophages. Murine peritoneal
macrophages were treated with peyote extract (0.18–18 µg/mL)
for 72 h, after which supernatants were collected to measure
nitrite levels, as explained in the text. Data represent means
of triplicate determinations from a representative experi-
ment (standard deviations were less than 1% of the means).
** p < 0.01, * p < 0.05 compared with medium alone (untreated
control), which did not stimulate nitrite release by macrophages.
murine lymphocytes and macrophages, and because
human macrophages possess limited capacity to pro-
duce nitric oxide, the effects of this extract were evalu-
ated on inflammatory cytokine gene expression and
viability of HPBMC. As observed in Fig. 3, peyote
extract increased IL-1β, IL-6 and IL-8 mRNA signals
by human leukocytes in a concentration-dependent
manner. Peyote extract at concentrations of 4.5, 9 and
18 µg/mL induced 0.15-, 0.99- and 1.85-fold increases in
IL-1 mRNA signal; 1.22-, 1.88- and 2.29-fold increases
Phytother. Res. 17, 1076–1081 (2003)
 IMMUNOPOTENTIATION BY LOPHOPHORA WILLIAMSII EXTRACT 1079

cells (house-keeping gene G3PDH signal was the same

for all experimental conditions, including the untreated
control (data not shown)). Peyote extract was also
observed not to alter human leukocytes viability (data
not shown).

Effect of L. williamsii extract on murine and human

tumour cell growth

The viability of L5178Y-R, U937, L929 and MCF7

Figure 3. Inflammatory cytokine gene expression of HPBMC by
L. williamsii extract. HPBMC were obtained and adjusted to 5 ×
106 cells/mL. Cytokine gene expression by human leukocytes
was then determined 5 h after addition of peyote extract, as
detailed in the text. Lane 1 represents leader 100 bp marker;
and lanes 2, 3 and 4 indicate cytokine mRNA signals induced
by peyote extract at 18, 9 and 4.5 µg/mL respectively. House-
keeping gene G3PDH signal was the same for all experimental
conditions, including the untreated control (data not shown).
in IL-6 mRNA signal, and 1.3-, 1.67- and 1.89-fold
increases in IL-8 mRNA signal respectively (Epi-Chemi
Darkroom, Labworks software v. 3, Ultra-Violet Prod-
ucts, Upland, CA) (Fig. 3), compared with unstimulated
tumour cell lines was significantly (p < 0.05) reduced
by L. williamsii extract (Fig. 4). MCF7 was the most
sensitive cell line to the cytotoxic effect of peyote
extract (concentration-dependent effect), which at
18 µg/mL, reduced its viability up to 1.3%; at this
extract concentration, viability of L5178Y-R, U937
and L929 cell lines was reduced up to 8%, 45% to
60%, respectively (Fig. 4).
DISCUSSION
Peyote has been used for centuries by Mexican Indians
(Huichol Indians) and Plains Indian Tribes of United
States and Canada such as the Navajo, Comanche, Sioux
and Kiowa as a ceremonial sacrament. Although pe-
yote was reported to possess teratogenic potential
if used in excess, it was not associated with abnor-
malities in lymphocyte chromosomes (Dorrance et al.,

Figure 4. Tumour cell growth inhibition by L. williamsii extract. Exponentially growing L5178Y-R (a), U937 (b), L929 (c), and MCF7
(d) cell line cultures were incubated for 72 h in the presence or absence of various concentrations (0.18–18 µg/mL) of L. williamsii
extract, as explained in the text. After incubation for 68 h, MTT was added to all wells, and cultures were incubated for an additional
4 h. Optical densities and percent viability were then determined by absorption at 540 nm as described in the text. Data represent
means of triplicate determinations from a representative experiment. ANOVA showed significant (p < 0.05) cytotoxic effect at all
concentrations of L. williamsii extract tested on these tumour cell lines. Optical density values for proliferation of untreated controls
were 1.119 ± 0.089, 0.847 ± 0.068, 1.376 ± 0.11 and 0.714 ± 0.058 for the tumour cell lines L5178Y-R, U937, L929 and MCF7,
respectively.

Copyright © 2003 John Wiley & Sons, Ltd. Phytother. Res. 17, 1076–1081 (2003)
1080 M. FRANCO-MOLINA ET AL.
1975). In the present study, it was shown that L.
williamsii extracts activated some parameters of immune
function of macrophages (nitric oxide and cytokine pro-
duction) and lymphocytes (proliferation), and were
cytotoxic to certain murine and human tumour cell lines
in vitro.
To our knowledge, this is the first report showing
that a methanol extract of peyote can not only potentiate
some immune parameters, but also directly kill tumour
cells. However, limited information on the immuno-
modulatory properties of peyote extracts or its bioactive
compounds is available. In this regard, mescaline
(peyote’s major active compound) has been shown
to inhibit in vitro concanavalin A-stimulated murine
lymphocyte proliferation (Sissors and Voss, 1978).
Activation of lymphoproliferation is relevant since
lymphocytes produce cytokines capable of stimulat-
ing lymphocyte and macrophage functions. In this
study, it was observed that peyote extract stimulated
lymphoproliferation in the absence of co-stimulatory
signals such as concanavalin A or LPS, without
significantly altering lymphocyte viability (Sissors and
Voss reported a reduction of viability in mescaline-
treated lymphocytes not greater than 20%, throughout
their experiments). However, Sissors and Voss’s study
cannot be compared with ours because our experi-
mental designs differed significantly. Although both
studies used Balb/c mice in the experiments, Sissors
and Voss utilized 5 × 10 6 splenic cells/mL (vs 1 × 107
thymic cells/mL by our group), 5 µg/mL concan-
avalin A-stimulated lymphocytes (we utilized resident
lymphocytes), and mescaline concentrations ranged
from 40 to 180 µg/mL (considering that mescaline
content in peyote usually averages 4% by dry weight,
there may have been mescaline concentrations in our
extract ranging from 0.0072 (0.18 µg/mL of the extract)
to 0.72 µg/mL (18 µg/mL of the extract)). There-
fore, the high concentrations of mescaline utilized
in Scissors and Voss’s experiments might have been
responsible for their observed effect on lymphopro-
liferation (they reported a reduction of lymphopro-
liferation ranging from 45% to 87%) (Sissors and Voss,
1978).
In the present study, it was shown that as the con-
centration of the extract was increased, there was a
decline in the lymphoproliferation index (Fig. 1); how-
ever, such a reduced response was still significantly
higher compared with the untreated control (Fig. 1). In
this regard, there might be some immunostimulatory
compounds in peyote’s extract whose concentration
might exceed that of a potential inhibitor of lympho-
proliferation, such as mescaline (Sissors and Voss, 1978),
thus masking its inhibitory effects. As the concentra-
tion of the extract was increased, it is possible that
substances such as mescaline, might alter lymphocyte
proliferation. More tests are necessary to chemically
characterize the peyote’s bioactive compounds, and to
elucidate the role of such substances, which may be
involved in both stimulation and inhibition of bio-
logical functions.
Peyote extract was also observed to directly activate
nitric oxide production by macrophages; however,
peyote was toxic for these cells. The observed toxicity
Copyright © 2003 John Wiley & Sons, Ltd.
of peyote for macrophages (up to 35% reduction of
viability at 18 µg/mL of peyote extract; the correla-
tion coefficient between nitric oxide production and
macrophage viability was 0.95) was probably due to
the action of peyote-induced nitric oxide (Albina
et al., 1993), rather than the direct action of peyote.
This was supported by the absence of peyote toxicity
towards murine lymphocytes and human leukocytes
(Fig. 3). Nitric oxide-mediated toxicity towards macro-
phages has been previously demonstrated by Albina
et al. (1993). They reported that stimulation of macro-
phages with 1 µg/mL LPS plus 10 U/mL IFN-γ caused
apoptosis of murine peritoneal macrophages (Albina
et al., 1993).
Peyote not only activated murine leukocytes (Figs 1
and 2), but also increased IL-1, IL-6 and IL-8 mRNA
signals in human mononuclear cells (Fig. 3), without
altering their viability (data not shown). These proteins
are extremely potent inflammatory molecules involved
in acute and chronic inflammation. Activation of in-
flammatory cytokines by peyote action on human cells
may be associated with their capacity to regulate the
development of certain types of cancer (Gough et al.,
2001). In this respect, it was shown that peyote extract
directly caused significant reduction in viability of
murine and human tumour cell lines (Fig. 4). MCF7
was the most sensitive cell line to the cytotoxic effect
of peyote extract (1.3% viability vs 8%, 45% to 60%
viability on L5178Y-R, U937 and L929 cells at 18 µg/mL
of peyote extract, respectively) (Fig. 4). Differences in
receptor type, density, affinity and modulation, protec-
tion receptor system, intracellular pathway activation,
and other mechanisms might have been involved in
the observed differential effects of peyote on growth of
these tumour cell lines.
In summary, it was shown in this study that peyote
extract was capable of stimulating lymphocyte pro-
liferation and killing tumour cells. However, it will be
necessary to elucidate this differential activity on
lymphocytes and tumour cells by isolating and testing
the bioactive compounds in peyote. In addition, it is
suggested that by activating lymphocyte and macro-
phage functions, peyote may have indirect (adjuvant)
antimicrobial properties (Gomez-Flores et al., 1997).
However, a direct antibiotic effect of peyote against
penicillin-resistant microorganisms, associated with
peyocactin and hordenine’s activity, has been reported
(Rao, 1970). Peyote’s antimicrobial action may be
associated with preventing infections and promoting
healing of Huichol Indians, who treat their wounds by
rubbing fresh peyote juices.
Plant products have been long known to possess
anticancer properties (Mukherjee et al., 2001). How-
ever, there is a continuing need for the development
of new anticancer drugs by screening natural pro-
ducts. There are still a number of plant compounds
that remain to be evaluated at the molecular, cellular
and physiological levels for their potential to treat
human diseases. Further studies are underway to
evaluate the methanol extract of peyote in vivo in a
murine cancer model, and to characterize the active
compound (s) that regulates immune function and
tumour cell growth.
Phytother. Res. 17, 1076–1081 (2003)
 IMMUNOPOTENTIATION BY LOPHOPHORA WILLIAMSII EXTRACT
REFERENCES
Albina JE, Cui S, Mateo RB, Reichner JS. 1993. Nitric oxide-
mediated apoptosis in murine peritoneal macrophages.
J Immunol 150: 5080–5084.
Borchers AT, Keen CL, Stern JS, Gershwin ME. 2000. Inflamma-
tion and Native American medicine: the role of botanicals.
Am J Clin Nutr 72: 339–347.
Dorrance DL, Janiger O, Teplitz RL. 1975. Effect of peyote on
human chromosomes. Cytogenetic study of the Huichol
Indians of Northern Mexico. JAMA 234: 299–302.
Gomez-Flores R, Rodriguez-Padilla C, Mehta RT, Galan-Wong L,
Mendoza E, Tamez-Guerra R. 1997. Nitric oxide and TNF-α
production by murine peritoneal macrophages activated
with a novel 20-kDa protein isolated from Bacillus thuring-
iensis var. thuringiensis parasporal bodies. J Immunol 158:
3796–3799.
Gomez-Flores R, Tucker SD, Kansal R, Tamez-Guerra R, Mehta
R. 1997. Enhancement of antibacterial activity of clofazimine
against Mycobacterium avium-M. intracellulare complex
infection induced by IFN-γ is mediated by TNF-α. J Anti-
microbial Chemother 39: 189–197.
Gough MJ, Melcher AA, Ahmed A, et al. 2001. Macrophages
orchestrate the immune response to tumor cell death.
Cancer Res 61: 7240–7247.
Hansen M, Nielsen S, Berg K. 1989. Re-examination and further
Copyright © 2003 John Wiley & Sons, Ltd.
1081
development of a precise and rapid dye method for measur-
ing cell growth/cell kill. J Immunol Methods 119: 203–210.
Hernandez-Pando R, Orozcoe H, Sampieri A, Alcocer JM,
Madrid Marina V. 1996. Correlation between the kinetics of
TH1/TH2 cells and pathology in a murine model of experi-
mental pulmonary tuberculosis. Immunology 89: 26–33.
Kaldjian EP, Chen GH, Cease KB. 1992. Enhancement of
lymphocyte proliferation assays by use of serum-free
medium. J Immunol Methods 147: 189–195.
Koenig HG. 2000. Psychoneuroimmunology and the faith
factor. J Gend Specif Med 3: 37–44.
McLaughlin JL. 1973. Peyote: an introduction. Lloydia 36: 1–8.
Mukherjee AK, Basu S, Sarkar N, Ghosh AC. 2001. Advances in
cancer therapy with plant based natural products. Curr Med
Chem 8: 1467–1486.
Rao GS. 1970. Identity of peyocactin, an antibiotic from peyote
(Lophophora williamsii), and hordenine. J Pharm Pharmacol
22: 544–545.
Roberts, TB. 1999. Do entheogen-induced mystical experiences
boost the immune system? Psychedelics, peak experiences,
and wellness. Adv Mind Body Med 15:139–147.
Sissors DL, Voss EW. 1978. Inhibition of lectin stimulation of
murine lymphocytes by mescaline. Biochem Pharmacol 27:
2705–2711.
Phytother. Res. 17, 1076–1081 (2003)