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Influence of virgin coconut oil (VCNO) on oxidative stress, serum testosterone and gonadotropic hormones (FSH, LH) in chronic ethanol ingestion

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  • University of Lagos (College of Medicine)

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The present study explored the effect of virgin coconut oil on oxidative stress, testosterone and gonadotropic hormones in alcohol-induced testicular injury. Twenty-five male rats were randomly assigned to one of five groups (n=5). The oil was processed from the mature endosperm of coconut and administered at 6.7 ml/kg body weight, while alcohol was given orally at 7 ml/kg body weight. After sacrifice, testicular malondialdehyde and serum hormone levels were determined. Testicular malondialdehyde levels increased significantly in animals treated with alcohol alone (p < 0.001), and animals treated with alcohol following virgin coconut oil treatment (p < 0.05) while the other groups showed a significant decrease (p < 0.05) when compared with the control. However, when compared with the group treated with alcohol alone, all the other groups showed a significant decrease (p < 0.05) in testicular malondialdehyde level. Serum testosterone levels increased significantly (p < 0.05) in rats treated with virgin coconut oil when compared with the alcohol-only treated group, while serum FSH and LH levels were not significantly different from the control values in all the treatment groups. Virgin coconut oil effectively lowered alcohol-induced oxidative stress by reducing testicular malondialdehyde levels and ameliorated the deleterious effect of alcohol on serum testosterone level, but showed no effect on serum FSH and LH levels.
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AGRICULTURE AND BIOLOGY JOURNAL OF NORTH AMERICA
ISSN Print: 2151-7517, ISSN Online: 2151-7525, doi:10.5251/abjna.2010.1.6.1126.1132
© 2010, ScienceHuβ, http://www.scihub.org/ABJNA
Influence of virgin coconut oil (VCNO) on oxidative stress, serum
testosterone and gonadotropic hormones (FSH, LH) in chronic ethanol
ingestion.
Dosumu, O. O., Duru, F. I. O., Osinubi, A. A., Oremosu, A. A., Noronha, C. C.
Department of Anatomy, Faculty of Basic Medical Sciences, College of Medicine,
University of Lagos, Idi-araba, Lagos, Nigeria
ABSTRACT
The present study explored the effect of virgin coconut oil on oxidative stress, testosterone and
gonadotropic hormones in alcohol-induced testicular injury. Twenty-five male rats were randomly
assigned to one of five groups (n=5). The oil was processed from the mature endosperm of
coconut and administered at 6.7 ml/kg body weight, while alcohol was given orally at 7 ml/kg
body weight. After sacrifice, testicular malondialdehyde and serum hormone levels were
determined. Testicular malondialdehyde levels increased significantly in animals treated with
alcohol alone (p < 0.001), and animals treated with alcohol following virgin coconut oil treatment
(p < 0.05) while the other groups showed a significant decrease (p < 0.05) when compared with
the control. However, when compared with the group treated with alcohol alone, all the other
groups showed a significant decrease (p < 0.05) in testicular malondialdehyde level. Serum
testosterone levels increased significantly (p < 0.05) in rats treated with virgin coconut oil when
compared with the alcohol-only treated group, while serum FSH and LH levels were not
significantly different from the control values in all the treatment groups. Virgin coconut oil
effectively lowered alcohol-induced oxidative stress by reducing testicular malondialdehyde levels
and ameliorated the deleterious effect of alcohol on serum testosterone level, but showed no
effect on serum FSH and LH levels.
Keywords: Virgin coconut oil, testes, testosterone, gonadotropic hormones
INTRODUCTION
Acute and chronic alcohol misuse or abuse has been
shown to cause derangements in reproductive
function in humans and experimental animals
(Mendelson et al., 1981; 1987; Little et al., 1992). The
male reproductive endocrine pathway consists of
three parts, hypothalamus, anterior pituitary and the
testes and is controlled through a classic negative
feedback mechanism (Emanuele & Emanuele, 1998).
Chronic ethanol consumption reportedly impacts all
levels of the male hypothalamic-pituitary-gonadal axis
(Van Thiel, 1983; Emanuele & Emanuele, 2001). It
also caused sexual dysfunction and impaired sperm
production in humans and in animal models (Van
Thiel & Lester, 1979).
Studies have shown that excessive ethanol ingestion
induces hypoandrogenism and hypogonadism in
males with low testosterone levels (Iturriaga et al.,
1995; Ren et al., 2005). In fact, research with animals
has consistently demonstrated an association
between both acute and chronic alcohol consumption
and low testosterone levels (Little et al., 1992;
Emanuele & Emanuele, 2001).
The oxidation of alcohol, a process that occurs as
part of alcohol metabolism generates by-products
called oxidants that can contribute to cell damage
and may play a role in alcohol-induced damage in the
testes (Bai & Cederbaum, 2006). Increased oxidative
stress is a well-accepted mechanism of alcohol-
induced tissue injury in the liver, heart and CNS
(Aleynik et al., 1998; Polavarapu et al., 1998) and it
has also been reported to occur in the testes
(Emanuele et al., 2001). Alcohol consumption may
induce oxidative damage either by enhancing the
production of toxic compounds called free radicals or
by decreasing the levels of antioxidants (Battino et
al., 1999; Dey & Cederbaum, 2006; Lu &
Cederbaum, 2008).
Coconut oil has been widely used throughout history
for its medicinal value and has served man as
important food for thousands of years (Ghazali et al.,
2009). It consists of a mixture of triglycerides
Agric. Biol. J. N. Am., 2010, 1(6): 1126-1132
containing only short and medium chain saturated
fatty acids (92%) and unsaturated fatty acids (8%)
(Reynolds, 1982; Dayrit, 2003; Che Mann & Marina,
2006).
The potential benefits of VCNO in preventing or
ameliorating different biological conditions due to its
active polyphenol components has been
demonstrated (Nevin & Rajamohan, 2004). The
extraction of VCNO from the fresh endosperm of
coconut is believed to be more beneficial than usually
prepared copra oil because its mode of extraction
retains more biologically active components such as
vitamin E and polyphenols (Nevin & Rajamohan,
2004). A recent study conducted by De Lourdes et al.
(2007) showed that despite increased testosterone
levels, CNO decreased the risk of prostatic cancer by
significantly reducing increase in prostate: body
weight ratio induced by testosterone. Though
research has reported the use of CNO in a number of
biological conditions, there is a dearth of literature on
its use as a pro-fertility agent. This has prompted the
present investigation.
MATERIALS AND METHODS
Animal experiments: Five groups of Sprague-
Dawley rats weighing between 100-150 g were used
for the study. The animals were housed with 12:12
light-dark cycle at 27 ± 1˚C in the animal house of the
department of anatomy, University of Lagos. The
experimental groups were divided into: Group I
(control); Group II (alcohol alone); Group III (alcohol
+ VCNO); Group IV (alcohol 8 weeks / VCNO 8
weeks); Group V (VCNO 8 weeks / alcohol 8 weeks).
VCNO was given at 6.7 ml/kg body weight per day
while alcohol was administered at 7 ml/kg body
weight per day following a modification of the
protocols described by Dayrit, (2000) and El-
Ashmawy et al. (2007) respectively. Both treatments
were given by gavage using a metal oropharyngeal
cannula as described in the protocols used by
Akinola et al. (2007) thrice in a week. Control animals
received normal saline throughout the duration of the
experiment. After 8 weeks treatment period, the
animals were sacrificed by cervical dislocation and
blood was obtained by ventricular puncture for
hormonal assay. The testes were dissected out,
trimmed of fat and used for the various assays.
Materials used: Alcohol: 30% ethanol prepared from
absolute ethanol (99.86% v/v) with substance
identification number 1170 manufactured by James
Burrough (F.A.D Ltd. UK) was used for the study.
Virgin coconut oil: The solid endosperm of mature
coconuts harvested between the months of
December-April (2009) and authenticated as Cocos
nucifera palmae at the Federal Institute of Forestry
Research Ibadan (Voucher number, 107825) were
used for the study.
The VCNO was extracted using a modified wet
extraction method described by Nevin and
Rajamohan, (2004, 2006). The solid endosperm of
mature coconut was crushed and made into a
viscous slurry. About 500 ml of water was added to
the slurry obtained and squeezed through a fine
sieve to obtain coconut milk. The resultant coconut
milk was left for about 24 hours to facilitate the
gravitational separation of the emulsion as previously
described by Onsaard et al., (2005) and Nour et al.,
(2009). Demulsification produced layers of an
aqueous phase (water) on the bottom, an emulsion
phase (cream) in the middle layer and an oil phase
on top as described by Nour et al. (2009). The oil on
top was scooped and heated for about 5 minutes to
remove moisture. The obtained VCNO was then
filtered through a fine sieve, stored at room
temperature and used for the experiment.
Biochemical Investigation
Determination of testicular malondialdehyde
levels: Lipid peroxidation as evidenced by the
formation of thiobarbituric acid reactive substances
(TBARS) was measured using the method described
by Niehaus and Samuelsson, (1968). A 0.1 ml tissue
homogenate (Tris-Hcl buffer, pH 7.5) was treated
with 2 ml of (1:1:1 ratio) TBA-TCA-HCL reagent
(Thiobarbituric acid 0.37%, 0.25N Hydrochloric acid,
and 15% Trichloroacetic acid [TCA]) and placed in
water bath for 15 minutes. Subsequently, the
samples were cooled and centrifuged at room
temperature for 10 minutes at 1000 rpm. The
absorbance of clear supernatant was measured
against reference blank at 535 nm. Concentration
was calculated using the molar absorptivity of
malondialdehyde, which is 1.56 x 105 M-1 cm-1.
Hormone determination: The serum levels of
testosterone, FSH and LH were measured using
commercially available enzyme-linked immunoassay
kit (Diagnostic automation Inc, CA) according to the
manufacturer’s instructions.
Statistical analysis: Statistical analysis was done
using student’s t test and analysis of variance
(ANOVA) with Bonferroni’s post hoc test. Data was
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expressed as means ± SD and p < 0.05 was
considered to be significant.
RESULTS
Testicular malondialdehyde level: tMDA levels
increased significantly in animals treated with alcohol
alone [Group II] (p < 0.001), and animals treated with
alcohol following VCNO treatment [Group V] (p <
0.05) while groups Groups III & IV showed a
significant decrease (p< 0.05) when compared with
the control. However when compared with the group
treated with alcohol alone, all the other groups
showed a significant decrease (p < 0.05) in tMDA
levels (Table I).
Table 1: Effect of the administration of VCNO and
alcohol on testicular malondialdehyde levels after eight
week-treatment regime.
Treatment Groups tMDA (nmol/min)
I (Control) 10.68 ± 1.04
II (ALC 8 WKS) 29.24 ± 2.51a
III (ALC + VCNO 8 WKS) 8.45 ± 1.07b
IV (ALC 8 WKS / VCNO 8
WKS) 6.62 ± 0.70b
V (VCNO 8 WKS / ALC 8
WKS) 18.01 ± 2.45b
Key
b: Significance at p < 0.05
a: Significance at p < 0.001
Serum hormone levels: When compared with the
control group, the alcohol-alone treated group
showed a significant reduction in testosterone levels
(p < 0.05), while groups III and IV that received
alcohol together with VCNO and VCNO following
alcohol treatment respectively showed a significant
increase (p < 0.05). Group V that received alcohol
following CNO treatment showed no significant
difference from the value of control. However, when
these groups were compared with the groups treated
with alcohol alone, they showed a significant increase
in testosterone levels (p < 0.05) (Figure 1).
When all the treated groups were compared with the
control as well as with the alcohol-only treated group,
both FSH and LH levels were not significantly
different (Figure 1).
Fig 1: Effect of VCNO and alcohol treatment on serum
TT, LH and FSH concentration in Sprague-Dawley rats
after 8 week-treatment regime.
y: p < 0.05 significant from values of II
Key
Group I - Control
Group III- ALC + CNO 8 WEEKS
Group II- ALC 8 WEEKS
Group V- CNO 8 WEEKS / ALC 8 WEEKS
Group IV- ALC 8 WEEKS / CNO 8 WEEKS
DISCUSSION
The effects of alcohol on testosterone and
gonadotropic hormones have been reported by
different authors. While Frias et al. (2000) reported
that alcohol ingestion produced a decrease in plasma
testosterone levels and no significant changes in
either FSH or LH levels; Little et al. (1992)
demonstrated that administration of alcohol to
prepubescent males stimulated testosterone
secretion with no changes in serum LH. Furthermore,
they stated that when alcohol was administered to
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adult male rats, both testosterone and LH levels
decreased.
In the studies of Ren et al. (2005) chronic exposure
of pubertal male rats to ethanol resulted in a decline
in serum testosterone level accompanied by a
decrease or “inappropriately” normal serum LH and
FSH levels, suggesting impaired secretory release of
gonadotropins. The present study agrees with these
findings as alcohol decreased serum testosterone
levels in the alcohol-only treated groups and showed
no significant changes in FSH and LH values in all
the rats.
Different authors have pointed out that although the
liver is the primary site for the breakdown of alcohol,
the testes also possesses the necessary enzymes. In
the presence of alcohol, these enzymes rather than
facilitate testosterone production are diverted to
alcohol breakdown, thus leading to a reduction in
testosterone levels over time (Ellingboe & Varanelli,
1979; Chiao et al., 2008). Studies have also shown
that alcohol consumption resulted in elevated levels
of the stress hormone, cortisol. Cortisol acts directly
on cells in the testes to inhibit the production and
release of testosterone, leading to suppressed
testosterone levels (Valmaki et al., 1984; Venkat et
al., 2009). These reasons could account for the
suppressed testosterone levels observed in the
alcohol-only treated groups.
While alcohol suppressed testosterone production in
the alcohol-only treated groups (group II), all the
groups treated with VCNO showed a significant
increase in serum testosterone levels when
compared with group II. This study agrees with the
findings of other authors who have reported that
animals fed CNO diets showed high testicular levels
of antioxidants in addition to significantly high levels
of testosterone and increase in the activities of 3-beta
or 17-beta dehydroxysteroid dehydrogenase
enzymes, key enzymes involved in testosterone
biosynthesis (Hurtado de Catalfo et al., 2008, 2009).
In the present investigation, tMDA levels were
elevated in the alcohol-only treated group, suggestion
a state of oxidative stress in the testes. However, the
administration of VCNO with alcohol ameliorated
these effects. Hence, this could also account for the
significant increase in testosterone levels observed in
the groups treated with VCNO when compared with
the alcohol-only treated groups. The studies of
Maneesh et al. (2006), have suggested that
increased oxidative stress caused damage to
testosterone secreting Leydig cells and supporting
Sertoli cells as well as impairing the HPG axis. In
addition, Calvin et al. (1981) suggested that the
metabolic pathway of testosterone synthesis requires
protection against peroxidation and will be affected
by a decrease in the activity of antioxidants. It is
therefore logical to believe that substances that could
ameliorate these effects will also boost testosterone
synthesis and release.
It is possible that the biologically active components
in VCNO such as tocotrienols (which have been
reported as having more potent antioxidant properties
than even alpha-tocopherol [Serbinova et al., 1991;
Serbinova & Packer, 1994]), flavonoids and other
polyphenols are responsible for the antioxidant
properties observed in this oil. Phenolics in particular
have been recognised as a powerful counter
measure against lipid peroxidation (Schroeter et al.,
2000; Ramos et al., 2005). Phenolic compounds can
act as free radical scavengers by virtue of their
hydrogen donating ability, forming aryloxyl radicals
(Dinkova-Kostova & Talalay, 1999). In addition,
phenolics have also been found interacting with the
oxidative cascade preventing its outcome
(Unnikishnan & Rao, 1992), quenching oxygen and
making it less available for oxidative reaction
(Soudamini et al., 1992). These antioxidant
properties demonstrated by VCNO may account for
its ability to decrease oxidative stress and prevent
tissue damage in the testes as well as protect the
metabolic pathway of testosterone against
peroxidation thereby preventing the suppression of
testosterone as observed in the alcohol-only treated
group.
Several mechanisms can account for the
“inappropriately” unchanged serum LH and FSH
levels observed in the present study and protein
retention has been sighted as one of them (Salonen
& Huhtaniem, 1990). Research on the liver has
demonstrated that short and long-term ethanol
exposure induces retention of nascent proteins
(Larkin et al., 1996). The ethanol-induced protein
retention in the liver resulted from impaired vesicle
transport and protein trafficking (Ghosh et al., 1995;
Torok et al., 1997).
Studies have shown that Rab proteins, a group of
small GTP proteins are important regulators of
transport of vesicles between the intracellular
organelles (Novick & Zerial, 1997; Segev, 2001;
Takai et al., 2001). When glycoproteins such as FSH
and LH move along the secretory pathway from the
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endoplasmic reticulum to plasma membrane, they
are contained in membrane limited vesicles
(Baenziger & Green, 1988). Reductions in these key
Rab proteins may lead to altered trafficking and may
play a role in disruption of pituitary FSH and LH
secretion. Studies of Ren et al. (2005) have shown
that ethanol decreases Rab protein levels in the
pituitary of treated rats. In agreement with these
findings, Tisdale et al. (1992) have reported that Rab
protein mutations inhibit vesicular transport, resulting
in protein accumulation.
Hence, chronic ethanol administration may affect
pituitary Rab proteins and disrupt the vesicle-
mediated secretory processes. Thus impaired
synthesis or secretion of LH and FSH could result,
explaining the inappropriately normal serum
gonadotropin levels observed in the study. It is
premature to conclude whether or not VCNO had any
effect on the gonadotropic hormones since the
duration of endocrinological recovery after alcohol
ingestion is a long-lasting process requiring different
times for different hormones to recover, during which
the normal glandular-pituitary feed-back process may
be partly put out of order (Ruusa et al., 1997).
Conclusion: In conclusion, we report that VCNO
effectively lowered alcohol-induced oxidative stress
by reducing tMDA levels and ameliorated the
deleterious effect of alcohol on serum testosterone
level, but showed no effect on serum FSH and LH
levels.
REFERENCES
Akinola, O. B., Dosumu, O. O., Akinleye, S. O. (2007). Effect of
cottonseed oil and Aloe vera supplement on the sperm
parameters of male wistar rats. The Journal of Health
Sciences, 14(2): 38-41.
Aleynik, S. I., Leo, M. A., Aleysink, M. K., Lieber, C. S.
(1998). Increasing circulating products of lipid
peroxidation in patients with alcoholic liver disease.
Alcoholism: Clinical and Experimental Research, 22:
192-196.
Baenziger, J. U., Green, E. D. (1988). Pituitary glycoprotein
hormone oligosaccharides: structure, synthesis and
function of the asparagine-linked oligosaccharides on
lutropin, follitropin and thyrotropin. Biochimica et
Biophysica Acta, 947: 287-306.
Bai, J., Cederbaum, A. I. (2006). Overexpression of
CYPSE1 in mitochondria sensitizes HepG2 cells to the
toxicity caused by depletion of glutathione. Journal of
Biological Chemistry, 281: 5128-5136.
Battino, M., Bullon, P., Wilson, M., Newman, H. (1999).
Oxidative injury and inflammatory periodontal
diseases: the challenge of anti-oxidants to free radicals
and reactive oxygen species. Critical Reviews in Oral
Biology and Medicine, 10: 458-476.
Calvin, H. I., Cooper, G. W., Wallace, E. (1981). Evidence
that selenium in rat sperm is associated with a cystine
rich structural protein of the mitochondrial capsule.
Gamete Research, 4: 139.
Che Man, Y. B., Marina, A. M. (2006). Medium chain
triacylglycerol. In F. Shaidi (ed.), Neutraceutical and
specialty lipids and their co-products (pg 27-56). Boca
Raton: Taylor and Francis Group.
Chiao, Y. B., Johnston, D. E., Gavaler, S. J., Van Thiel, D.
H. (2008). Efect of chronic feeding on testicular
content of enzymes required for testosteronogenesis.
Alcoholism: Clinical and Experimental Research, 5(2):
230-236.
Dayrit, C. S. (2000). Coconut oil in health and disease: Its
monolaurin potential as cure for HIV / AIDS. XXXVII
Cocotech meeting, Chennai, India.
Dayrit, C. S. (2003). Cococnut oil: Atherogenic or Not?
(What therefore causes Atherosclerosis?), Philippine
Journal of Cardiology, 31(3): 97-104.
De Lourdes, A. M., Molina, V., Más, R., Carbajal, D.,
Marrero, D., Gonzalez, V., Rodriguez, E. (2007).
Effects of coconut oil on testosterone-induced prostatic
hyperplasia in Sprague-Dawley rats. The Journal of
Pharmacy and Pharmacology, 59(7): 995-999.
Dey, A., Cederbaum, A. I. (2006). Alcohol and oxidative
liver injury. Hepatology, 43: S63-S74.
Dinkova-kostova, H. and Talalay, P. (1999). Relation of
structure of curcumin analogs to their potencies as
inducers of phase-2 detoxification
enzymes. Carcinogenesis, 20: 911-914.
El-Ashmawy, I. M., Saleh, A., Salama, O. M. (2007). Effects
of marjoram volatile oil and grape seed extract on
ethanol toxicity in male rats. Basic and Clinical
Pharmacology and Toxicology, 101(5): 328-332.
Ellingboe, J., Varanelli, C. C. (1979). Ethanol inhibits TT
biosynthesis by direct action on Leydig cells. Research
Communications in Chemical Pathology and
Pharmacology, 24(1): 87-102.
Emanuel, M. A., and Emanuel, N. V. (2001). Alcohol and
the male reproductive system. Alcohol Research and
Health, 25(4): 282-287.
1130
Agric. Biol. J. N. Am., 2010, 1(6): 1126-1132
Emanuele, M., A. and Emanuele, N., V. (1998). Alcohol
effects on male reproduction. Alcohol Health and
Research World, 22(3): 195-201.
Emanuele, N. V., Lapagli, N., Steiner, J., Colantoni, A., Van
Thiel, D. H., Emanuele, M. A. (2001). Peripupertal
paternal EtOH exposure. Endocrine, 14(2): 213-219.
Frias, J., Rodriguez, R., Torres, J. M., Ruiz, E., Ortega, E.
(2000). Effects of acute alcohol intoxication on pituitary
gonadal axis hormones, pituitary adrenal axis
hormones, beta-endorphin and prolactin in human
adolescents of both sexes. Life Sciences, 67: 1081-
1086.
Ghazali, H. M., Tan, A., Abdulkarim, S. M., Dzulkifly, M. H.
(2009). Oxidative stability of virgin coconut oil compared
with RBD palm olein in deep-fat frying of fish crackers.
Journal of Food and Environment, 7(3-4): 23-27.
Ghosh, P., Liu, Q. H., Lakshman, M. R. (1995). Long-term
ethanol exposure impairs glycosylation of both N- and
O-glycosylated proteins in rat liver. Metabolism 44:
890-898.
Hurtado de Catalfo, G. E., de Alaniz, M. S., Marra, C. A.
(2008). Dietary lipids modify redox homeostasis and
steroidogenic status in rat testis. Nutrition, 24(7-8):
717-726.
Hurtado de Catalfo, G. E., de Alaniz, M. S., Marra, C. A.
(2009). Influence of commercial dietary oils on lipid
composition and TT production in interstitial cells
isolated from rat testis. Lipids, 44(4): 34-357.
Iturriaga, H., Valladres, L., Hirsch, S., Devoto, E., Perez,
C., Bunout, D. L., Lioi, X., Petermann, M. (1995).
Effects of abstinence on sex hormone profile in
alcoholic patients without liver failure. Journal of
Endocrinological Investigation, 18(8): 638-644.
Larkin, J. M., Oswald, B., McNiven, M. A. (1996). Ethanol-
induced retention of nascent proteins in rat
hepatocytes is accompanied by altered distribution of
the small GTP-binding protein rab2, Journal of Clinical
Investigation, 98: 2146-2157.
Little, P. J., Adams, M. L., Cicero, T. J. (1992). Effect of
alcohol on the hypothalamic pituitary gonadal axis in
the developing male rat. Journal of Pharmacology and
Experimental Therapeutics, 263: 1056-1061.
Lu, Y., Cederbaum, A. I. (2008). CYP2E1 and oxidative
liver injury by alcohol. Free Radical Biology and
Medicine, 44: 723-738.
Maneesh, M., Dutta, S., Chakrabarti, A., Vasuderan, D. M.
(2006). Alcohol abuse-duration dependent decrease in
plasma TT and antioxidants in males. Indian Journal of
Physiology and Pharmacology, 50(3): 291-296.
Mendelson, J. H., Mello, N. K., Cristofano, P., Ellingboe, J.,
Skupny, A., Palmieri, S. L., Benedikt, R., Schiff, I.
(1987). Alcohol effects on naloxone-stimulated LH,
prolactin and estradiol in women. Journal of Studies in
Alcohol, 48: 287-294.
Mendelson, J. H., Mello, N. K., Ellingboe, J. (1981). Acute
alcohol intake and pituitary gonadal hormones in
normal human females. Journal of Pharmacology and
Experimental Therapeutics, 218: 23-26.
Nanji, A. A., Sadrzadeh, S. M., Yang, E. K., Fogt, F.,
Maydani, M., Dannenberg, A. J. (1995). Dietary
saturated fatty acids: a novel treatment for alcoholic
liver disease. Gastroenterology, 109: 547-554.
Nevin, K. G., Rajamohan, T. (2004). Beneficial effects of
virgin coconut oil on lipid parameters and in vitro LDL
oxidation. Clinical Biochemistry, 37(9): 830-835.
Nevin, K. G., Rajamohan, T. (2006). Virgin coconut oil
supplemented diet increases the antioxidant status in
rats. Food Chemistry, 99(2): 260-266.
Niehaus, W. G., Samuelsson, B. (1968). Formation of
malondialdehyde from phospholipid arachidonate
during microsomal lipid peroxidation. European
Journal of Biochemistry, 6: 126-130.
Nour, A. H., Mohammed, F. S., Yunus, R. M., Arman, A.
(2009). Demulsification of virgin coconut oil by
centrifugation method: A feasibility study. International
Journal of Chemical Technology, 1(2): 59-64.
Novick, P., Zerial, M. (1997). The diversity of Rab proteins
in vesicle transport. Current Opinion in Cell Biology, 9:
496-504.
Onsaard, E., Vittayanont, M., Srigam, S., McClements, D.
J. (2005). Properties and stability of oil-in-water
emulsions stabilized by coconut skim milk proteins.
Journal of Agriculture and Food Chemistry, 53: 5747-
5753.
Polavarapu, R., Spitz, D. R., Sim, J. E., Follansbee, M.H.,
Oberley, L. W., Rahemtulla, A. (1998). Increased lipid
peroxidation and impaired antioxidant enzyme function
is associated with pathological liver injury in
experimental alcoholic liver disease in rats fed diets
high in corn oil and fish oil. Hepatology, 27: 1317-
1323.
Ramos, S., Alia, M., Bravo, L., Goya, L. (2005).
Comparative effects of food-derived polyphenols on
the viability and apoptosis of a human hepatoma cell
line (HepG), Journal of Agricultural and Food
Chemistry, 53: 1271-1280.
1131
Agric. Biol. J. N. Am., 2010, 1(6): 1126-1132
1132
Ren, J. C., Zhu, Q., Lapaglia, N., Emanuele, N. V.,
Emanuele, M. A. (2005). Ethanol-induced alterations in
Rab proteins: possible implications for pituitary
dysfunction. Alcohol, 35 (2): 103-112.
Reynolds, J. E. F., (ed.,), (1982). Martindale: The Extra-
Pharmacopoeia (28th ed). The Pharmaceutical Press,
London, pp 695-698.
Ruusa, J., Bergman, B., Sundell, M. L. (1997). Sex
hormones during alcohol withdrawal: a longitudinal
study of 29 male alcoholics during detoxification.
Alcohol and Alcoholism, 32(5): 591-597.
Salonen, I., Huhtaniemi, I. (1990). Effects of chronic
ethanol diet on pituitary-testicular function of the rat,
Biology of Reproduction, 42: 55-62.
Schroeter, H., Williams, R. J., Martin, R., Iversen, L., Rice E.
(2000). Phenolic antioxidants attenuate neuronal cell
death following uptake of oxidised low density
lipoprotein. Free Radical Biology and Medicine, 29:
1222-1233.
Segev, N. (2001). Ypt/rab gtpases: regulators of protein
trafficking. Science Signalling: Signal Transduction
Knowledge Environment, 2001(100): re11.
Serbinova, E. A., Kagan, V., Han, D., Packer, L. (1991).
Free radical recycling and intramembrane mobility
inthe antioxidant properties of alpha-tocopherol and
alpha-tocotrienol. Free Radical Biology and Medicine,
10(5): 263-275.
Serbinova, E. A., Packer, L. (1994). Antioxidant properties
of alpha-tocopherol and alpha-tocotrienol. Methods in
Enzymology, 234: 354-366.
Soudamini, K. K., Unnikrishnan, M. C., Soni, K. B., Kuttan,
R. (1992). Inhibition of lipid peroxidation and
cholesterol levels in mice by curcumin. Indian Journal
of Physiology and Pharmacology, 36: 239-243.
Takai, Y., Sasaki, T., Matozaki, T. (2001). Small GTP-
binding proteins. Physiological Reviews, 81: 153-208.
Tisdale, E. J., Bourne, J. R., Khosravi-Far, R., Der, C. J.,
Balch, W. E. (1992). GTP-binding mutants of rab1 and
rab2 are potent inhibitors of vesicular transport from
the endoplasmic reticulum to the Golgi complex.
Journal of Cell Biology, 119: 749-761.
Torok, N., Marks, D., Hsiao, K., Oswald, B. J., McNiven, M.
A. (1997). Vesicle movement in rat hepatocytes is
reduced by ethanol exposure: alterations in
microtubule-based motor enzymes. Gastroenterology,
113: 1938-1948.
Unnikrishnan, M. K., and Rao, M. N. A. (1992). Curcumin
inhibits nitrite induced methemoglobin formation. The
FEBS Journal, 301: 195-196.
Välimäki, M. J., Härkönen, M., Eriksson, C. J., Ylikahri, R.
H. (1984). Sex hormones and adrenocortical steroids
in men acutely intoxicated with ethanol. Alcohol, 1(1):
89-93.
Van Thiel, D. H. (1983). Ethanol: Its adverse effects upon
the hypothalamus pituitary gonadal axis. Journal of
Laboratory and Clinical Medicine, 101(1): 21-33.
Van Thiel, D. H., Lester, R. (1979). The effect of chronic
alcohol abuse on sexual function. Clinical
Endocrinology and Metabolism, 8: 499-510.
Venkat, K. K., Arora, M. M., Singh, P., Desai, M.,
Khatkhatay, I. (2009). Effect of alcohol consumption on
bone mineral density and hormonal parameters in
physically active male soldiers. Bone, 45(3): 449-454.
... One of these plant lipid or olis is VCO. Virgin coconut oil contains saturated and unsaturated fatty acids (Dosumu et al., 2010). Lauric acid represents 50% of the total fatty acids, which is considered as antibacterial, antiviral and anti-inflammatory component (Zakaria et al., 2011). ...
... The glycerol interferes with the intracellular ice crystal formation and hence protects spermatozoa from cryo-injury (Holt, 2000;Hammerstedt et al., 1990). Moreover, virgin coconut oil has a high percentage of saturated fatty acids (Dosumu et al., 2010) and solidifies at 20°C, which could clarify the difficulty of using concentrations of more than 8% in the extenders. Higher VCO caused a solid floating 'lid' of oil in the test tube after chilling at 5°C, due to non-emulsified oil and this finding was similar to that of del Valle et al. (2013). ...
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The aim of this study was to assess the effects of virgin coconut oil (VCO) combined with coconut milk (CM) on chilled and frozen-thawed quality parameters of bull sperm. Twenty four semen samples were collected from four bulls. Samples were diluted in Tris extender containing 0% (negative control only 3% (CM) in Tris-base extender), 2%, 4%, 6%, 8% VCO mixed with 3% CM and 20% egg yolk (positive control). Extended samples were divided into two fractions, one was chilled at 4°C for 24, 72 and 144 hours and the second fraction packed into 0.25 ml straws and frozen in liquid nitrogen for 7 and 14 days. Subsequently, chilled samples and the straws were thawed and evaluated for sperm motility by Computer Assisted Semen Analyzer (CASA), viability, acrosome integrity, morphology (eosin-nigrosin) and membrane integrity (hypo-osmotic swelling test). Higher (p < 0.05) percentage of sperm parameters was observed in the positive control group in chilled semen, followed by 8% VCO compared to the other concentrations of the VCO. There was no significant difference in morphology between positive control and all other treatment groups in chilled or frozen-thawed semen. The positive control group was higher in all sperm parameters measured when compared with treated groups in frozen-thawed semen. In conclusion, the results showed that the mixture of VCO with coconut milk applied in this study could not maintain the function of bull sperm after chilled and frozen-thawed better than the positive control.
... These PUFA are formed from linoleic acid (LA), and they give fluidity to the sperm plasma membrane, which helps in the fusion events of fertilization. More recently, antioxidants (AOX) and Phytosterols (PST), commonly found in substantial amounts in special oils, such as Pecan nut (PNO) Corn (CO) and grape seed (GSO) oils 7,8 . These oils are associated with a lower risk of inflammation, dyslipidemia, and low risk of oxidative stress required for the maintenance of endothelial integrity 9,10 . ...
... oil and groundnut oil. At the same time, the same results were found in our study (7,13) . In the same study, the virgin coconut oil and HARRT showed a significant reduction in the diameter of seminiferous tubules; moreover, there was no effect on the germinal layer. ...
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Objective: To evaluate the protective role of virgin coconut oil and corn oil in phenytoin induced toxicity of rat on the basis of histomorphology of seminiferous tubules. Study Design: Experimental study Place and Duration of Study: This study was conducted at the department of Anatomy of Al-Tibri Medical College and Hospital, for a period of six months from October 2018 to November 2019. Materials and Methods: 48 numbers of male albino rats were randomly selected with weight between 150-250gms. Four different groups were made on the basis of therapeutic agents. Group A control, Group B phenytoin induced intra-peritoneal, Group C virgin coconut oil plus phenytoin and Group D corn oil plus phenytoin. The sample was taken by given anesthesia and both testes were removed through dissection at 4th, 5th and 6th week. The sample was preserved for tissue processing and staining. Tubular dimension were measured through micrometry at 400x, mean of five different tubules from five different field areas were taken and one way ANOVA followed by post hoc tukeys test was applied to evaluate the significant difference among different groups. P value considered to be significant <0.05 Results: Mean value of tubular dimension was significantly reduced in phenytoin induced toxic group, while in group A and C shows significant restoration of tubular dimension as compared to group D on three different week. Conclusion: Virgin coconut oils showed significant restoration of seminiferous tubules dimension when used along with phenytoin for 6 weeks in comparison of corn oil. Virgin coconut oil showed significant ant oxidative effects and alter the toxic effects of drugs if administered simultaneously
... This thus reverses the damage to sperm quality and testicular tissue. This is in line with the reports on the ameliorative effect of coconut oil on reproductive function (40). ...
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Sperm quality is impaired in diabetic conditions. Coconut oil (CO) possesses anti-diabetic properties and ameliorative effects on testicular dysfunction. Lauric acid (LA) being the most abundant constituent of CO is hypothesized to be responsible for its physiologic actions. This study investigated some testicular and sperm parameters in diabetic male wistar rats treated with lauric acid and coconut oil. Thirty animals were divided into six groups of five each. Group I: Control; Group II: Diabetic untreated; Group III: Diabetic treated with LA (90 mg/Kg). Group IV: Diabetic treated with LA (180 mg/Kg); Group V: Diabetic treated with LA (360 mg/Kg). Group VI: Diabetic treated with CO (1.42 ml/Kg). Compared to Group I, there was a significant decline (p < 0.05) in gonadosomatic index, serum testosterone level, sperm quality and testicular structure in Group II. Compared to Group II; the gonadosomatic index, sperm quality were significantly higher (p < 0.05) in Group VI. Compared to Group II; Group V and Group III had significantly higher (p < 0.05) percentages of normal and progressively motile sperm cells respectively. Testicular histoarchitecture was improved in Groups 5 and 6. Sperm quality was largely improved by coconut oil but not by lauric acid. This contradicts the assumption that lauric acid may be largely credited for this physiologic action of coconut oil.
... It helps in controlling blood sugar level as it preserves insulin action and insulin resistance. VCO also helps in preventing liver disease by reversing hepatosteatosis which is a type of fatty liver disease [10,11]. Moreover, coconut oil also plays important roles in hair care and cosmetic products. ...
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Virgin coconut oil is a useful substance in our daily life. It contains a high percentage of lauric acid which has many health benefits. The current industry has developed several methods to extract the oil out from the coconut fruit. This review paper aims to highlight several common extraction processes used in modern industries that includes cold extraction, hot extraction, low-pressure extraction, chilling, freezing and thawing method, fermentation, centrifugation, enzymatic extraction and supercritical fluid carbon dioxide. Different extraction methods will produce coconut oil with different yields and purities of lauric acid, thus having different uses and applications. Challenges that are faced by the industries in extracting the coconut oil using different methods of extraction are important to be explored so that advancement in the oil extraction technology can be done for efficient downstream processing. This study is vital as it provides insights that could enhance the production of coconut oil.
... p-Coumaric acid, ferulic acid, caffeic acid, and catechin acid are the major phenolic acids found in CO (Marina et al., 2009a). VCO is also rich in active polyphenol compounds, which are strong inhibitors of lipid peroxidation (Dosumu et al., 2010). Polyphenols are known for their neuroprotective actions, especially in preventing the neurotoxic effects of β-amyloid (Menard et al., 2013). ...
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Dementia is a general term for loss of memory, language, problem-solving, and other thinking abilities that are severe enough to interfere with daily life. Alzheimer's disease (AD) is the most common cause of dementia. Risk factors as age, genetics, environment, lifestyle, and metabolic disease. The etiology of AD remains not fully explained, but both genetic and environmental risk factors have been proposed to be involved. Microscopically, intraneuronal neurofibrillary tangles (NFTs) and extracellular senile plaques characterize the AD. The amyloid cascade hypothesis (ACH) suggests that the imbalance between the Amyloid-β generation and its clearance causes dysfunction and consequently cell death. Coconut oil may represent a cheap and natural treatment for AD. This is because coconut oil contains medium-chain triglycerides (MCTs), which are digested to ketones in the liver that are linked to mitochondrial function enhancement and oxidation-reduction. Recent studies have investigated the possibility of using trans-zeatin and phytoestrogen and other sex hormones like substances present in coconut water and a young coconut juice (YCJ) in reducing the chance of AD. Coconut is known as a 'functional food' that is extremely nutritious. Virgin coconut oil (VCO) differs from ordinary coconut oil as the former contains a lot more biologically active components. Phenolic compounds and hormones contained in coconut can help prevent amyloid b peptide aggregation, potentially inhibiting a key step in the pathogenesis of AD. Coconut can be useful in the treatment of obesity, dyslipidemia, elevated low-density lipoproteins, insulin resistance, and hypertension-these are the risk factors for chronic venous disease and type II diabetes, as well as for AD.
... Ethanol treatment results in a significant TBARS increase in the testes and an insignificant one in the liver, kidneys and brain. These findings are in accordance with other investigations showing that acute and chronic exposure to ethanol administered either orally, or intraperitoneally leads to increased free radical and lipid peroxide formation in rat testes (4,8,15). Thus, ROS generation and lipid peroxidation might be an important mechanism of ethanol toxicity in the testes (1,13,14). ...
... Meanwhile, the results of a study on the effect of VCO administration for 30 days on the hematological parameters of mice showed an increase in SOD enzyme levels [17]. VCO at a dose of 6.7 ml / kgBW can reduce testicular MDA levels in rats induced by giving alcohol a dose of 7 ml / kgBW [18]. The results of the study reported that VCO given acutely can increase endurance rats at maximal physical activity [19]. ...
... Alcohol has been reported to reduce serum/plasma testosterone level in experimental animals [23,24,25,26]. In men, low androgen level has also been reportedly associated with both moderate consumptions with chronic alcohol consumption [27,28,29,30]. ...
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Locally brewed alcoholic beverages have become part of the socioeconomic life of the Nigerian and West African communities. The negative effect of the use of the beverages on both health, economic and social life is worth exploring amidst the increasing challenges of poverty, inadequate health facilities, lack of basic social amenities amongst many others. This study aimed at evaluating the effect of some selected locally brewed Nigerian alcoholic beverage on the hormonal profile of male and female albino rats. A total of 60 screened rats (spaque Dawley strain) of body weight 180-200g and comprising 30 males and females each were randomly divided into five groups of six animals of same sex per cage and administered with various doses of local alcoholic beverages-goskolo, burukutu, pito and ogogoro per oral for a period of 21 days. Serum hormonal assays were carried out with the use of the respective EIA Kit, ELISA microwells and microplate immunoassay. Results revealed significant decrease (p < 0.05) in the sex hormones (estrogen, progesterone, and testosterone) in all the male treated with these alcoholic beverages, while LH and FSH were not significantly affected. The toxicological evaluation of traditional alcoholic beverages pito, burukutu, ogogorogo and goskolo revealed significant decrease in the sex hormonal profile of male and female albino rats. This buttressed the toxicological effect by way of decrease in the activity of the sex hormones necessary for fertility and reproduction the rats.
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Pefloxacin (PEF) has been reported to cause most fluoroquinolone-associated tendinopathy while recent studies show that exogenous supplementation with micro-nutrients facilitate recovery of tendinopathy. Virgin coconut oil (VCO) has been reported to modulate antioxidant enzyme activities, pro-inflammation, and apoptosis. The aim of this study was to determine if VCO would prevent or reverse the damage of PEF on tendon morphology and structure. Material and Method. Fifty (50) male Sprague-Dawley rats were randomized into four main categories designated as Normal control, Experimental control, Prophylactic and Treatment groups. All animals in the experimental groups were orally administered PEF 400mg/kg of body weight in a fixed volume of 2.5 ml/kg body weight once daily for 6 consecutive days. The prophylactic groups had prior administration of VCO (V.PEF) at a dosage of 6.7 ml/kg body weight for 7 consecutive days while the treatment groups had the VCO after PEF (PEF.V). All the animals were serially sacrificed on days 8, 15 and 22 and the tendons excised and processed. Data were analyzed with RSTUDIO version 4.0.02 and data normality in the Control and Experimental groups were tested using Shapiro Wilk normality test. Level of significance was 0.5. Results. Kruskal Wallis showed significant differences (p < 0.05) in all the biomechanical parameters across all the groups. Days 8 and 15 comparisons of the biomechanics of the tendons in the experimental groups showed no significant (p > 0.05) differences except the day 22 groups (p= 0.028). The PEF and PEF.V tendons had severely compromised biomechanical properties on day 8, with improvements observed from day 15 while the V.PEF group showed better properties as early as day 8 which continued till 15 th day. Conclusion: VCO given prophylactically ameliorated the damage of PEF on the tendon while it significantly improved biomechanical properties from day 15 when given post PEF.
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Full-text available
Pefloxacin (PEF) has been reported to cause most fluoroquinolone-associated tendinopathy while recent studies show that exogenous supplementation with micro-nutrients facilitate recovery of tendinopathy. Virgin coconut oil (VCO) has been reported to modulate antioxidant enzyme activities, pro-inflammation, and apoptosis. The aim of this study was to determine if VCO would prevent or reverse the damage of PEF on tendon morphology and structure. Material and Method. Fifty (50) male Sprague-Dawley rats were randomized into four main categories designated as Normal control, Experimental control, Prophylactic and Treatment groups. All animals in the experimental groups were orally administered PEF 400mg/kg of body weight in a fixed volume of 2.5 ml/kg body weight once daily for 6 consecutive days. The prophylactic groups had prior administration of VCO (V.PEF) at a dosage of 6.7 ml/kg body weight for 7 consecutive days while the treatment groups had the VCO after PEF (PEF.V). All the animals were serially sacrificed on days 8, 15 and 22 and the tendons excised and processed. Data were analyzed with RSTUDIO version 4.0.02 and data normality in the Control and Experimental groups were tested using Shapiro Wilk normality test. Level of significance was 0.5. Results. Kruskal Wallis showed significant differences (p < 0.05) in all the biomechanical parameters across all the groups. Days 8 and 15 comparisons of the biomechanics of the tendons in the experimental groups showed no significant (p > 0.05) differences except the day 22 groups (p= 0.028). The PEF and PEF.V tendons had severely compromised biomechanical properties on day 8, with improvements observed from day 15 while the V.PEF group showed better properties as early as day 8 which continued till 15 th day. Conclusion: VCO given prophylactically ameliorated the damage of PEF on the tendon while it significantly improved biomechanical properties from day 15 when given post PEF.
Article
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The oxidative stability of virgin coconut oil (VCO) in deep fat frying at 185 ± 5°C for a total of 30 hours was evaluated and compared with that of similarly-treated RBD palm olein (RBDPO) based on changes in the peroxide value (PV), p-anisidine value (p-AV), total oxidation (TOTOX) value, total polar compound (TPC) content and color. The sample used in the frying study is a favorite Malaysian snack, fish crackers, a dried product comprising mainly of sago starch and comminuted fish. Twenty grams of the crackers were fried for 60-90 seconds in 1.5 kg of oil, 12 batches a day at an interval of 5 minutes, for five consecutive days. On each day of frying, fresh oil was added to replenish the oil used to its original volume before the next frying was carried out. Results show that there was a significant increase (P
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The keratinous capsules surrounding rat sperm mitochondria were isolated 24 days after intratesticular injections of [75Se] selenite or [35S] cysteine. Dodecyl sulfate-polyacrylamide gel electrophoresis of purified, doubly labeled mitochondrial capsules revealed only a single 75Se-labeled component, whose molecular weight was 17,000, in agreement with previously reported observations obtained with cruder sperm fractions. Most of the 35S label and the major zone of stained protein on the gels coincided with the position of 75Se, suggesting that selenium is associated with a cysteine-rich structural protein. The level of selenium in rat sperm, 195 ± 3.2 ng/108 sperm (approximately 30 ppm), determined by hydride generation and atomic absorption spectrophotometry, is consistent with a structural function for this trace element in the sperm.
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Virgin coconut oil (VCO) directly extracted from fresh coconut meat at 50°C temperature was tested for its effect on the activities of antioxidant enzymes and lipid peroxidation levels in male Sprague–Dawley rats, compared to copra oil (CO) and groundnut oil (GO) as control. Oils were fed to rats for 45 days along with a semi-synthetic diet and after the experimental period various biochemical parameters were done. Individual fatty acid analyses of VCO and CO were done using gas chromatography. Effect of polyphenol fraction isolated from the oils was also tested for the ability to prevent in vitro microsomal lipid peroxidation induced by FeSO4. The results showed that GO, rich in polyunsaturated fatty acids, reduced the levels of antioxidant enzymes and increased lipid peroxidation, indicated by the very high MDA and conjugate diene content in the tissues. PF fraction from VCO was found to have more inhibitory effect on microsomal lipid peroxidation compared to that from the other two oils. VCO with more unsaponifiable components viz. vitamin E and polyphenols than CO exhibited increased levels of antioxidant enzymes and prevented the peroxidation of lipids in both in vitro and in vivo conditions. These results showed that VCO is superior in antioxidant action than CO and GO. This study has proved that VCO is beneficial as an antioxidant.
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The coconut is called the tree of life for it has been providing us, humans, food and drink, materials for housing, fuel and many industrial uses. And its medicinal uses are many and varied. The latest medical potential of products of the coconut first identified by Jon Kabara and others in the 70s, is the anti-bacterial, anti-viral and anti-fungal activity of its medium chain fatty acids, particularly lauric acid (C12:0) in its monoglyceride form (monolaurin or ML).
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Rab proteins have been primarily implicated in vesicle docking as regulators of SNARE pairing. Recent findings, however, indicate that their function in vesicle trafficking can go beyond this role, and a number of proteins, unrelated to each other, have been identified as putative Rab effectors. Although the GTPase switch of Rab proteins is highly conserved, functional mechanisms may be highly diversified among members of the Rab family.
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Consumption of fruits and vegetables, which are rich in polyphenols, has been associated with a reduced risk of chronic diseases such as cancer. Dietary polyphenols have antioxidant and antiproliferative properties that might explain their beneficial effect on cancer prevention. The aim of this study was to investigate the effects of different pure polyphenols [quercetin, chlorogenic acid, and (-)-epicatechin] and natural fruit extracts (strawberry and plum) on viability or apoptosis of human hepatoma HepG2 cells. The treatment of cells for 18 h with quercetin and fruit extracts reduced cell viability in a dose-dependent manner; however, chlorogenic acid and (-)-epicatechin had no prominent effects on the cell death rate. Similarly, quercetin and strawberry and plum extracts, rather than chlorogenic acid and (-)-epicatechin, induced apoptosis in HepG2 cells. Moreover, quercetin and fruit extracts arrested the G1 phase in the cell cycle progression prior to apoptosis. Quercetin and strawberry and plum extracts may induce apoptosis and contribute to a reduced cell viability in HepG2 cells.