Protective effects of AA and NAC in pancreatitis

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Protective effects of AA and NAC in pancreatitis

Post Number:#1  Post by ofonorow » Sun Jul 15, 2012 3:02 am

Ultrastructural clues for the protective effect of ascorbic acid and N-acetylcysteine against oxidative damage on caerulein-induced pancreatitis.
http://www.ncbi.nlm.nih.gov/pubmed/16864970

RESULTS:

Formation of vacuoles, mitochondrial damage, and dilatation of rough endoplasmic reticulum, margination and clumping of chromatin were major ultrastructural alterations in AP group. Ascorbic acid + NAC prevented these changes. Small vacuoles were present within the cytoplasm of some of the acinar cells. Pancreas damage was accompanied by an increase in tissue malondialdehyde (MDA) levels (p < 0.05), whereas a decrease was seen in catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) activities and total glutathione (GSH) levels (p < 0.005). Ascorbic acid + NAC decreased MDA levels but increased CAT, SOD, GPx activities and GSH levels (p < 0.005).

CONCLUSION:

These results suggest that ascorbic acid + NAC is potentially capable of limiting pancreatic damage produced during AP via protecting fine structure of acinar cells and tissue antioxidant enzyme activities.


Still looking for evidence (proof) that NAC alone can increase intracellular GSH, and the problem is that all (most) animal models make their own ascorbate. This study in rats, which presumably make their own ascorbate.
Owen R. Fonorow, Orthomolecular Naturopath
My statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”

ofonorow
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Re: Protective effects of AA and NAC in pancreatitis

Post Number:#2  Post by ofonorow » Sun Jul 15, 2012 3:08 am

Put your thinking caps on (if this abstract is correct) as it implies that NAC reduced the factor (NRF2) that increases GSH production in cells? The increase in GSH was assumed, thus to be because of Reactive Oxygen Species (ROS).

Differential induction of apoptosis in human breast cancer cell lines by phenethyl isothiocyanate, a glutathione depleting agent.
http://www.ncbi.nlm.nih.gov/pubmed/22351438

Phenethyl isothiocyanate (PEITC) is a naturally occurring electrophile which depletes intracellular glutathione (GSH) levels and triggers accumulation of reactive oxygen species (ROS).

PEITC is of considerable interest as a potential chemopreventive/chemotherapeutic agent, and in this work, we have investigated the effects of PEITC on human breast cancer cell lines. Whereas PEITC readily induced apoptosis in MDA-MB-231 cells (associated with rapid activation of caspases 9 and 3, and decreased expression of BAX), MCF7 cells were relatively resistant to the apoptosis promoting effects of PEITC.

The relative resistance of MCF7 cells was associated with high basal expression of NRF2, a transcription factor that coordinates cellular protective responses to oxidants and electrophiles and raised intracellular levels of GSH.

This raised basal expression of NRF2 appeared to be a response to on-going production of ROS, since treatment with the antioxidant and GSH precursor N-acetylcysteine (NAC) reduced NRF2 expression.

Moreover, pre-treatment of MDA-MB-231 cells with NAC rendered these cells relatively resistant to PEITC-induced apoptosis. In summary, our data confirm that PEITC may be an effective chemopreventive/therapeutic agents for breast cancer. However, differences in the basal expression of NRF2 and resultant changes in GSH levels may be an important determinant of sensitivity to PEITC-induced apoptosis.
Owen R. Fonorow, Orthomolecular Naturopath
My statements have not been evaluated by the Food and Drug Administration. Any product mentioned is not intended to diagnose, treat, cure or prevent any disease.”


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