Dithiolthiones are phytochemicals in the class of Organosulfides, found abundantly in cruciferous vegetables, garden sorrel, horseradish, etc.
Health Benefits
1. Anti acetaminophen hepatotoxicity
In the investigation of Anethol dithiolthione
(ADT), usually prescribed as a choleretic drug, given orally 1 hour
prior to acetaminophen (AAP) (450 mg/kg intraperitoneally) in Swiss
female mice, found that ADT exhibited an hepatoprotective potency at
doses as low as 10 mg/kg relative to serum aminotransferase activities
and hepatic glutathione related enzyme system (glutathione reductase,
peroxidase, transferase), according to "Protective effect of anethol dithiolthione against acetaminophen hepatotoxicity in mice" by Warnet JM, Christen MO, Thevenin M, Biard D, Jacqueson A, Claude JR.(1)
2. Chemopreventive efficacy
in
the observation of two exposure regimens used to compare the efficacies
of early (Regimen-A) versus late (Regimen-B) intervention in
prevention of lung tumorigenesis in A/J mice, indicated that Evaluation
of lung tumor multiplicity following exposure to oltipraz showed that
oltipraz inhibited the tumor development in a dose-dependent manner
(10-100 mg/m(3)) with inhibition ranging from 37 to 53% in Regimen A
and 51% in Regimen B, when compared with the B[a]P group. Analysis of
the tumor incidence showed that 81.5% of the animals had 10 or more
tumors in the B[a]P group, whereas, in oltipraz exposure groups, there
was a significant decrease in Regimen A (24-36%) and in Regimen B
(42%), according to "The chemopreventive efficacy of inhaled oltipraz particulates in the B[a]P-induced A/J mouse lung adenoma model" by Sharma S, Gao P, Steele VE.(2)
3. Detoxication of xenobiotics
In
the testing The dithiolthiones, oltipraz, ADT, 116L and 129L, in mice
and in rats, oltipraz. Intragastric administration of dithiolthiones
(oltipraz, ADT or 116L; two doses each of 1 g/kg body weight) found that
Dithiolthiones present in cabbage may play a role in the protective
actions of diets high in vegetables against the toxic actions of
xenobiotics, according to "Biochemical effects of dithiolthiones' by Ansher SS, Dolan P, Bueding E.(3)
4. Antioxidants
In
the examination of the role of glutathione (GSH) in the regulation of
this adhesion phenomenon and in the increased tyrosine phosphorylation
induced by ROS, found that ADT reduced both PMN adhesion to
ROS-stimulated human umbilical vein endothelial cells (HUVEC) and
tyrosine phosphorylation of p125FAK and paxillin. ADT increased redox
status by increasing intracellular GSH content in oxidized cells. These
results show that GSH can reverse the effect of oxidation on tyrosine
kinase activation and phosphorylation, and thus plays an important role
in cell signaling. They also confirm the antioxidant activity of ADT,
according to "Anethole dithiolethione regulates oxidant-induced tyrosine kinase activation in endothelial cells" by Ben-Mahdi MH, Gozin A, Driss F, Andrieu V, Christen MO, Pasquier C.(4)
5. Aflatoxin B1 contamination
In the study of the influence of oltipraz and a second dithiolthione,
(1,2) dithiolo (4,3-c)-1,2-dithiole-3,6 dithione (DDD) on bovine
hepatic aflatoxin B1 biotransformation, found that Oltipraz inhibited
aflatoxin B1 metabolism as no aflatoxin M1 and no aflatoxin
B1-dihydrodiol, the second metabolite found in bovine hepatocytes, was
formed. DDD did not significantly inhibit aflatoxin B1 metabolism. It
could be demonstrated that the inhibition of aflatoxin B1 metabolism
was due to the inhibition of several cytochrome P450 enzyme activities
by oltipraz. In contrast, DDD inhibited only ethoxyresorufin
O-deethylation activity, according to "Inhibition of aflatoxin M1 production by bovine hepatocytes after intervention with oltipraz" by Kuilman ME, Maas RF, Woutersen-van Nijnanten FM, Fink-Gremmels J.(5)
6. Cancer prevention
In
the investigation of The critical role of the glutathione S-transferase
(GST) and their importance in cancer prevention and susceptibility,
clinical studies revealed that the GST activity of blood lymphocytes
from individuals with either a personal or family history of colorectal
cancer or a personal history of colon polyps was decreased
significantly when compared to that of healthy controls. Phase 1
clinical evaluation of oltipraz has demonstrated its ability to induce
GST activity as well as the level of transcripts encoding
gamma-glutamylcysteine synthetase (gamma-GCS) and DT-diaphorase in the
colon mucosa of individuals at increased risk for colorectal cancer.
The observed correlation between the posttreatment response in blood
lymphocytes and colon mucosa suggested that blood lymphocytes may be
used in future trials as a surrogate biomarker of the responsiveness of
colon tissue to chemopreventive regimens, according to "Glutathione S-transferases--biomarkers of cancer risk and chemopreventive response" by Clapper ML, Szarka CE.(6)
7. Anti nephrotoxicity
in
the determination of s the effects of ADT on hexachloro-1,3-butadiene
(HCBD)-induced nephrotoxicity in the rat and the mechanism of its
action, found that ADT protects rats against HCBD-induced nephrotoxicity
by a mechanism that does not involve the modulation of HCBD
conjugation with liver GSH, nor the modulation of the kidney NPSH level
and beta-lyase activity. The mechanism of protection conferred to rats
by an ADT pretreatment against HCBD-induced nephrotoxicity appears to
take place in the kidney at a step beyond the generation of ultimate
toxic metabolites derived from PCBC, according to 'Assessment of the role of glutathione conjugation in the protection afforded by anethol dithiolthione against hexachloro-1,3-butadiene-induced nephrotoxicity" by Bouthillier L, Charbonneau M, Brodeur J.(7)
8. Inhibition of platelet aggregation
in the investigation of Anethole dithiolthione
(ADT) (10 mumol/l) inhibition of platelet aggregation and the
formation of thromboxane (Tx)B2 in plasma in response to adenosine
diphosphate (ADP), epinephrine and arachidonic acid (AA), indicated
that ADT had no additive effect on the inhibition of thrombin-induced
platelet aggregation by acetylsalicylic acid. ADT was a more effective
inhibitor of AA-induced platelet aggregation than butylated
hydroxytoluene. ADT inhibited the release of 3H-AA from platelet
phospholipids in response to ADP and collagen. It is suggested that ADT
inhibits platelet aggregation by inhibiting thromboxane synthesis and
preventing AA release, according to "Effect of anethole dithiolthione on human platelet aggregation" by Selley ML, McGuiness JA, Bartlett MR, Ardlie NG.(8)
9. Early colon carcinogenesis
in
the study of the effect of dietary oltipraz on liver and colonic
mucosal enzymes and DNA adducts in evaluating the modulating role of
this agent during the early period of azoxymethane (AOM)-induced
carcinogenesis, showed that dietary oltipraz enhances the colonic and
liver glutathione S-transferase activity and reduced the formation of
DNA adducts. In addition, dietary oltipraz modulates liver and colonic
ODC and TPK activities that have been shown to play a role in tumor
promotion, according to "Effect of
oltipraz [5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione] on
azoxymethane-induced biochemical changes related to early colon
carcinogenesis in male F344 rats" by Rao CV, Nayini J, Reddy BS.(9)
10. Lipid peroxidation
in
the observation of the drug anisyldithiolthione (ADT) acted as a good
inhibitor of lipid peroxidation induced in rat liver microsomes either
chemically by FeSO4 and reducing agents (cysteine or ascorbate) or
enzymatically by NADPH and CC14, showed that at doses as low as 5 mg
per kg it completely suppressed ethane exhalation by
acetaminophen-intoxicated mice and also protected them very efficiently
against mortality caused by acetaminophen overdose. The inhibitory
effect of ADT toward lipid peroxidation seems to be linked to the
presence of its dithiolthione function, according to "A new potent inhibitor of lipid peroxidation in vitro and in vivo, the hepatoprotective drug anisyldithiolthione" by Mansuy D, Sassi A, Dansette PM, Plat M.(10)
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Sources
(1) http://www.ncbi.nlm.nih.gov/pubmed/2780509
(2) http://carcin.oxfordjournals.org/content/27/8/1721.abstract
(3) http://www.ncbi.nlm.nih.gov/pubmed/3744194
(4) http://www.ncbi.nlm.nih.gov/pubmed/11213483
(5) http://www.ncbi.nlm.nih.gov/pubmed/10682385
(6) http://www.ncbi.nlm.nih.gov/pubmed/9679568
(7) http://www.ncbi.nlm.nih.gov/pubmed/8685901
(8) http://www.ncbi.nlm.nih.gov/pubmed/1497692
(9) http://www.ncbi.nlm.nih.gov/pubmed/2020672
(10) http://www.ncbi.nlm.nih.gov/pubmed/3964266
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