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26 février 2011 6 26 /02 /février /2011 10:19

Free Radic Biol Med. 2011 Jan 31. [Epub ahead of print]

S-allylmercapto-N-acetylcysteine up-regulates cellular glutathione and protects vascular endothelial cells from oxidative stress.

Izigov NFarzam NSavion N.


Oxidative stress and/or low cellular glutathione (GSH) levels are associated with the development and progression of numerous pathological conditions. Cells possess various antioxidant protection mechanisms, including GSH and phase II detoxifying enzymes. N-acetylcysteine (NAC) supplies cells with cysteine to increase GSH level but its efficacy is relatively low because of its limited tissue penetration. Allicin (diallyl thiosulfinate), a reactive sulfaorganic compound, increases cellular GSH and phase II detoxifying enzymes in vascular endothelial cells (EC). A novel compound was designed: S-allylmercapto-N-acetylcysteine (ASSNAC), a conjugate of S-allyl mercaptan (a component of allicin) and NAC. Both ASSNAC and NAC increased cellular GSH of ECs, reaching a maximum of up to four- and threefold increase after exposure for 24 or 6h at a concentration of 0.2 or 1mM, respectively. ASSNAC induced nuclear translocation of the activated transcription factor Nrf2 and expression of phase II detoxifying enzymes. EC exposure to tBuOOH resulted in 75% cytotoxicity, and pretreatment of cultures with 0.2mM ASSNAC or 2mM NAC reduced cytotoxicity to 20 and 42%, respectively. In conclusion, ASSNAC is superior to NAC in protecting cells from oxidative stress because of its ability to up-regulate both GSH and the expression of phase II detoxifying enzymes.

Copyright © 2011 Elsevier Inc. All rights reserved.

PMID: 21281712 [PubMed - as supplied by publisher]

 

 

Eur J Nutr. 2009 Mar;48(2):67-74. Epub 2008 Dec 1.


Allicin up-regulates cellular glutathione level in vascular endothelial cells.


Horev-Azaria LEliav SIzigov NPri-Chen SMirelman DMiron TRabinkov AWilchek MJacob-Hirsch JAmariglio NSavion N.

Goldschleger Eye Research Institute, Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.

BACKGROUND: Allicin in garlic is the primary active compound known to rapidly interact with free thiols.

AIMS OF THE STUDY: To examine the effect of allicin on gene expression and glutathione cellular level in vascular endothelial cells.

METHODS: Cultured endothelial cells were exposed to allicin; mRNA was prepared and subjected to Micro-array and Real-Time PCR. Glutathione cellular level was determined on cell lysates.

RESULTS: Micro-array analysis demonstrated allicin-induced up- and down-regulation of 116 and 100 genes, respectively. Up-regulated genes included the phase II detoxifying enzymes thioredoxin reductase 1 and 2, heme oxygenase-1 and glutamate cysteine lygaze modifier subunit, the rate limiting enzyme in glutathione biosynthesis. Endothelial cells exposed to allicin and its derivatives containing glutathione or cysteine residues increased cellular glutathione. Allicin increased the glutathione level in a concentration and time-dependent manner up to 8-fold at a concentration of 10-20 microM after 28 h exposure. Furthermore, allicin derivative-treated cultures demonstrated a 50% decrease in tBuOOH cytotoxicity.

CONCLUSIONS: These results may suggest a putative role for allicin and its derivatives in preventing reactive oxygen species damage by up-regulating the phase II detoxifying enzymes and increasing the cellular glutathione level.

PMID: 19048328 [PubMed - indexed for MEDLINE]

 

 

Eur J Appl Physiol. 2008 Jun;103(3):275-83. Epub 2008 Feb 28.

Effects of allicin supplementation on plasma markers of exercise-induced muscle damage, IL-6 and antioxidant capacity.

Su QSTian YZhang JGZhang H.

Chengdu Physical Education University, No.2 Ti-Yuan Road, 610041 Chengdu, China. sqs111@126.com

To investigate the effects of allicin supplementation on exercise-induced muscle damage (EIMD), interleukin-6 (IL-6), and antioxidative capacity, a double-blinded, placebo-controlled study was conducted in well-trained athletes. Subjects were randomly assigned to an allicin supplementation group (AS group) and a control group, and received either allicin or placebo for 14 days before and 2 days after a downhill treadmill run. Plasma creatine kinase (CK), muscle-specific creatine kinase (CK-MM), lactate dehydrogenase (LDH), IL-6, superoxide dismutase (SOD), total antioxidative capacity (TAC), and perceived muscle soreness were measured pre and post exercise. AS group had significantly lower plasma levels of CK, CK-MM and IL-6, and reduced perceived muscle soreness after exercise, when compared with the control group. AS group also demonstrated a trend toward reducing plasma concentration of LDH after exercise (P = 0.08), although not statistically significant. Allicin supplementation induced a higher value of TAC at rest, and this higher value was maintained 48 h after exercise, however, there was no difference in SOD values after exercise between the two groups. The results suggested that allicin might be a potential agent to reduce EIMD. Further studies concerning anti-inflammatory and anti-oxidative effects of allicin on EIMD are needed.

PMID: 18305954 [PubMed - indexed for MEDLINE]

 


 


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