For those with IBS, Crohn's, IBD, gastritis, etc.
- From: "montygram" <nazztrader@xxxxxxxxx>
- Date: 4 May 2005 21:34:39 -0700
One thing your doctor probably never told you was to avoid unsaturated
fatty acids, especially certain oils (corn, vegetable, soy, canola,
sunflower, safflower, etc.), yet the evidence is overwhelming. You can
go to www.pubmed.com and do various searches, for example crohn
oxidative will bring up all but the first, which came from
www.sciencedaily.com:
5/2/2005
Food Fried In Vegetable Oil May Contain Toxic Compound
MINNEAPOLIS / ST. PAUL -- University of Minnesota researchers A. Saari
Csallany, a professor of food chemistry and nutritional biochemistry,
and graduate student Christine Seppanen have shown that when highly
unsaturated vegetable oils are heated at frying temperature (365 F) for
extended periods--or even for half an hour--a highly toxic compound,
HNE (4-hydroxy-trans-2-nonenal) forms in the oil.
Previously, vegetable oils such as soybean, sunflower and corn were
regarded as heart-healthy because of their high levels of linoleic
acid, a polyunsaturated fatty acid. HNE is incorporated into fried food
in the same concentration as it forms in the heated oil. Also, Csallany
and her colleagues have found three toxic HNE-related compounds (known
as HHE, HOE and HDE) in heated soybean oil. They will present their
work at a poster session from 9 a.m. to 2 p.m. Wednesday, May 4, at the
96th annual meeting of the American Oil Chemists Society in the Salt
Lake City Convention Center.
"HNE is a well known, highly toxic compound that is easily absorbed
from the diet," said Csallany. "The toxicity arises because the
compound is highly reactive with proteins, nucleic acids--DNA and
RNA--and other biomolecules. HNE is formed from the oxidation of
linoleic acid, and reports have related it to several diseases,
including atherosclerosis, stroke, Parkinson's, Alzheimer's,
Huntington's and liver diseases."
Csallany's work underscores the risk of repeated heating, or reusing,
highly unsaturated oils for frying because HNE accumulates with each
heating cycle. In future studies, Csallany and her colleagues plan to
determine how long polyunsaturated oil must be heated at lower
temperatures in order to form HNE and its related compounds. The study
was funded by the University of Minnesota.
Am J Physiol Gastrointest Liver Physiol. 2004 Apr;286(4):G528-37. Epub
2003 Dec 4.
Linoleic acid induces interleukin-8 production by Crohn's human
intestinal smooth muscle cells via arachidonic acid metabolites.
Alzoghaibi MA, Walsh SW, Willey A, Yager DR, Fowler AA 3rd, Graham MF.
Department of Physiology, Virginia Commonwealth University, Richmond,
Virginia 23298-0034, USA. swwalsh@xxxxxxx
Previously we reported that linoleic acid (LA), but not oleic acid,
caused a marked increase in the secretion of IL-8 by Crohn's human
intestinal smooth muscle (HISM) cells. Antioxidants inhibited this
response, implicating a role for oxidative stress and NF-kappaB, a
transcription factor for IL-8 that is activated by oxidative stress. In
this study, we examined two mechanisms whereby LA, the dietary
precursor for arachidonic acid (AA), could increase the production of
IL-8 via activation of AA pathways: 1) by generation of reactive oxygen
species by the AA-pathway enzymes to activate NF-kappaB or 2) by AA
metabolites. Normal and Crohn's HISM cells were exposed to LA,
oxidizing solution (Ox), or oxidizing solution enriched with LA (OxLA).
Exposure of cells to Ox or OxLA induced oxidative stress as determined
by thiobarbituric acid reactive substances. In normal cells, Ox but not
LA activated NF-kappaB as determined by transfection experiments and
Western blot. In Crohn's cells, NF-kappaB was spontaneously activated
and was not further activated by Ox or LA. In contrast, TNF-alpha
markedly increased activation of NF-kappaB in both normal and Crohn's
cells. These results indicated that LA did not increase IL-8 by
activating NF-kappaB, so we evaluated the second mechanism of an effect
of AA metabolites. In normal cells, OxLA, but not LA, markedly
stimulated IL-8, whereas in Crohn's cells, both OxLA and LA stimulated
IL-8. OxLA, also stimulated production of AA metabolites leukotriene
B(4) (LTB(4)), PGE(2), and thromboxane B(2) (TXB(2)) by normal and
Crohn's cells. To determine whether AA metabolites mediated the IL-8
response, cells were treated with OxLA plus indomethacin (Indo), a
cyclooxygenase inhibitor, and nordihydroguaiaretic acid (NDGA), a
lipoxygenase inhibitor. Both Indo and NDGA blocked the IL-8 response to
OxLA. To determine more specifically a role for AA metabolites, AA was
used. Similar to OxLA, OxAA stimulated production of IL-8 and AA
metabolites. Pinane thromboxane, a selective thromboxane synthase
inhibitor and receptor blocker, inhibited OxAA stimulation of TXB(2)
and IL-8 in a dose-response manner. MK886, a selective 5-lipoxygenase
inhibitor, inhibited OxAA stimulation of LTB(4) and IL-8 also in a
dose-response manner. Analysis of specific gene products by RT-PCR
demonstrated that HISM cells expressed receptors for both thromboxane
and LTB(4). We conclude that AA metabolites mediated the IL-8 response
to LA in HISM cells. Both cyclooxygenase and lipoxygenase pathways were
involved. LA did not increase IL-8 by activating NF-kappaB, but
NF-kappaB appeared to be involved, because LA increased IL-8 only in
situations where NF-kappaB was activated, either spontaneously in
Crohn's cells or by Ox in normal cells. We speculate that AA
metabolites increased IL-8 production by enhancing NF-kappaB-dependent
transcription of IL-8.
Cell Stress Chaperones. 2003 Winter;8(4):329-34.
Expression of heat shock protein 32 (hemoxygenase-1) in the normal and
inflamed human stomach and colon: an immunohistochemical study.
Barton SG, Rampton DS, Winrow VR, Domizio P, Feakins RM.
Department of Adult and Paediatric Gastroenterology, Barts and the
London, Queen Mary School of Medicine and Dentistry, London E1 2AD, UK.
Heat shock protein 32 (Hsp32, hemoxygenase-1) is induced by reactive
oxygen metabolites (ROM) and degrades heme leading to the formation of
antioxidant bilirubin. Increased mucosal generation of ROM occurs in
gastritis and inflammatory bowel disease. We aimed to assess mucosal
expression of Hsp32 in normal stomach and colon and to test the
hypothesis that disease-related differential expression occurs in
inflamed tissue. Gastric body and antral mucosal biopsies were obtained
from 33 patients comprising Helicobacter pylori-negative normal
controls (n = 8), H pylori-negative gastritis patients (n = 11), and H
pylori-positive gastritis patients (n = 14). Forty-seven archival
colonic mucosal biopsies selected comprised normal histology (n = 10),
active ulcerative colitis (UC) (n = 9), inactive UC (n = 8), active
Crohn's disease (CD) (n = 8), inactive CD (n = 6), and other colitides
(n = 6). Hsp32 expression in formalin-fixed sections was assessed by
avidin-biotin peroxidase immunohistochemistry using a polyclonal rabbit
anti-Hsp32 as the primary antibody. Immunohistochemical staining
identified Hsp32 in all groups. Diffuse cytoplasmic staining was seen
in gastric and colonic epithelial and lamina proprial inflammatory
cells. Staining scores for Hsp32 were higher in antral H
pylori-positive (P = 0.002) and H pylori-negative (P = 0.02) gastritis
than in controls and in body H pylori-positive gastritis than in the
other 2 groups (P < 0.01). Expression of Hsp32 was increased in active
UC compared with inactive disease (P = 0.03) and normal controls (P =
0.02). In conclusion, Hsp32 is expressed constitutively in normal
gastric and colonic mucosa, and differential expression occurs in these
tissues when they are inflamed. Upregulation of Hsp32 may be an
adaptive response to protect mucosa from oxidative injury in patients
with gastritis and inflammatory bowel disease.
Dig Dis Sci. 2004 Sep;49(9):1433-7.
Decreased total and corrected antioxidant capacity in patients with
inflammatory bowel disease.
Koutroubakis IE, Malliaraki N, Dimoulios PD, Karmiris K, Castanas E,
Kouroumalis EA.
Department of Gastroenterology, University Hospital Heraklion, P.O. Box
1352, Heraklion 71110, Greece. ktjohn@xxxxxxxxxxxxxxx
Oxidative stress and depletion of antioxidants may play a key role in
the pathogenesis of inflammatory bowel disease (IBD)-related intestinal
damage. A new automated assay for the determination of blood total
antioxidant capacity (TAC), based on the crocin bleaching method, has
been used for the measurement of TAC and corrected TAC (cTAC) in
patients with ulcerative colitis (UC) and Crohn's disease (CD) in
comparison to healthy controls (HC). Ninety-four patients with UC, 97
patients with CD, and 72 HC were included in this study. Serum TAC was
measured in all patients and controls on an Olympus AU-600 chemistry
analyzer using a TAC kit. cTAC was calculated from TAC after
subtraction of the interactions due to endogenous uric acid, bilirubin
and albumin. Mean serum TAC as well as cTAC levels were significantly
lower in both UC and CD patients compared with HC (P < 0.0001).
Patients with active UC had no different TAC and cTAC compared to those
with inactive disease. Patients with active CD had significantly lower
mean TAC compared to those with inactive disease but cTAC was not
different between the two phases of disease activity. Patients with
proctitis had significantly higher TAC and cTAC compared to patients
with left-sided colitis and total colitis. In CD patients no
association between disease localization and these markers was found.
TAC and cTAC are significantly reduced in IBD patients compared with
controls irrespective of disease activity. The decreased antioxidant
defenses may be a primary phenomenon severely compromising the mucosa
and therefore increase susceptibility to oxidative tissue damage.
World J Gastroenterol. 2005 Jan 21;11(3):403-6.
Lipid peroxidation and antioxidant status in colorectal cancer.
Skrzydlewska E, Sulkowski S, Koda M, Zalewski B, Kanczuga-Koda L,
Sulkowska M.
Department of Analytical Chemistry, Medical University of Bialystok,
Mickiewicza 2, 15-230 Bialystok, Poland. skrzydle@xxxxxxxxxx
AIM: Reactive oxygen species (ROS) can induce carcinogenesis via DNA
injury. Both enzymatic and non-enzymatic parameters participate in cell
protection against harmful influence of oxidative stress. The aim of
the present study was to assess the levels of final lipid peroxidation
products like malondialdehyde (MDA) and 4-hydroxy-2-nonenal (4-HNE) in
primary colorectal cancer. Moreover, we analysed the activity of main
antioxidative enzymes, superoxide dismutase (Cu, Zn-SOD), catalase
(CAT), glutathione peroxidase (GSH-Px) and glutathione reductase
(GSSRG-R) and the level of non-enzymatic antioxidants (glutathione,
vitamins C and E). METHODS: Investigations were conducted in 81 primary
colorectal cancers. As a control, the same amount of sample was
collected from macroscopically unchanged colon regions of the most
distant location to the cancer. Homogenisation of specimens provided
10% homogenates for our evaluations. Activity of antioxidant enzymes
and level of glutathione were determined by spectrophotometry. HPLC
revealed levels of vitamins C and E and served as a method to detect
terminal products of lipid peroxidation in colorectal cancer. RESULTS:
Our studies demonstrated a statistically significant increase in the
level of lipid peroxidation products (MDA-Adc.muc.-2.65+/-0.48 nmol/g,
Adc.G3-2.15+/-0.44 nmol/g, clinical IV stage 4.04+/-0.47 nmol/g,
P<0.001 and 4-HNE-Adc.muc. -0.44+/-0.07 nmol/g, Adc.G3-0.44+/-0.10
nmol/g, clinical IV stage 0.52+/-0.11 nmol/g, P<0.001) as well as
increase of Cu,Zn-SOD (Adc.muc.-363+/-72 U/g, Adc.G3-318+/-48 U/g,
clinical IV stage 421+/-58 U/g, P<0.001), GSH-Px (Adc.muc. -2143+/-623
U/g, Adc.G3-2005+/-591 U/g, clinical IV stage 2467+/-368 U/g, P<0.001)
and GSSG-R (Adc.muc.-880+/-194 U/g, Adc.G3-795+/-228 U/g, clinical IV
stage 951+/-243 U/g, P<0.001) in primary tumour comparison with normal
colon (MDA-1.39+/-0.15 nmol/g, HNE-0.29+/-0.03 nmol/g, Cu,
Zn-SOD-117+/-25 U/g, GSH-Px-1723+/-189 U/g, GSSG-R-625+/-112 U/g)
especially in mucinous and G3-grade adenocarcinomas as well as clinical
IV stage of colorectal cancer. We also observed a decrease of CAT
activity (Adc.muc. -40+/-14 U/g, clinical IV stage 33+/-18 U/g vs
84+/-17 U/g, P<0.001) as well as a decreased level of reduced
glutathione (clinical IV stage 150+/-48 nmol/g vs 167+/-15 nmol/g,
P<0.05) and vitamins C and E (vit. C-clinical IV stage 325+/-92 nmol/g
vs 513+/-64 nmol/g, P<0.001; vit. E-clinical IV stage 13.3+/-10.3
nmol/g vs 37.5+/-5.2 nmol/g). CONCLUSION: Colorectal carcinogenesis is
associated with serious oxidative stress and confirms that gradual
advancement of oxidative-antioxidative disorders is followed by
progression of colorectal cancer.
.
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