Posted: Mon Nov 09, 2009 6:00 am
NAC boosts the natural antioxidant capacity of the cells by increasing glutathione concentrations, which is one of the main natural antioxidant enzymes.
sou
sou
Welcome to This is MS, the leading forum for Multiple Sclerosis research and support. Join our friendly community of patients, caregivers, and researchers celebrating over 20 years of delivering hope through knowledge.
https://www.thisisms.com/forum/
I have exactly same problem.wonky1 wrote:I love green tea, unfortunately it makes me vomit. I think I've damaged my stomach lining with one pill or another.
That's what i also discovered in my research about Green Tea as it contains high amounts of fluoride as i was worried about consuming tons of that toxic mineral daily and so i assume the ECGC supplements are fluoride free correct?zap wrote:I am not sure about the extracts, but tea - especially cheaper green tea leaves, is incredibly high in sodium fluoride, which does seem to effect the BBB/endothelium.
http://www.google.com/search?q=tea+sodium+fluoride
http://www.google.com/search?q=endothel ... m+fluoride
I drink tea, but I avoid cheaper teas (made with older leaves) and drink in moderation.
The following posts may be of interest if you haven't already seen them yet. They discuss fluoride and tea.harry1 wrote:That's what i also discovered in my research about Green Tea as it contains high amounts of fluoride as i was worried about consuming tons of that toxic mineral daily and so i assume the ECGC supplements are fluoride free correct?
Thanks everyone !!!
Clin Exp Pharmacol Physiol. 2009 Jul;36(7):612-8.
Endoplasmic reticulum stress involved in heart and liver injury in iron-loaded rats.
Lou LX, Geng B, Chen Y, Yu F, Zhao J, Tang CS.
Institute of Cardiovascular Diseases, Peking University First Hospital, Beijing, China.
1. Iron overload contributes to the pathogenesis of various diseases and directly induces tissue injury. In the present study, we investigated the relationship between heart and liver injury induced by iron overload and cellular endoplasmic reticulum (ER) stress to explore the molecular mechanism of iron overload-induced cellular injury. 2. Iron overload in rats was generated by intraperitoneal injection of iron-dextran chronically (30 mg/kg per day for 9 weeks) or acutely (300 mg/kg once). Tissue injury was assessed by determining serum lactate dehydrogenase (LDH), alanine aminotransferase (ALT) and aspartate aminotransferase (AST) activity, as well as malondialdehyde (MDA) content in the heart and liver. The ER stress response was analysed by expression of glucose-response protein 78 (GRP78) and activation of caspase 12. 3. In chronic iron-loaded rats, iron levels in the heart and liver were higher, by approximately 2- and 7.8-fold, respectively (P < 0.01), compared with control. Serum LDH, ALT and AST activity, as well as MDA content, GRP78 expression and caspase 12 activity in the heart and liver, were upregulated in chronically iron-loaded rats. In acute iron-loaded rats, iron content in the heart and liver was 51% and 63% higher than in controls (both P < 0.01). Serum LDH, ALT and AST activity, MDA content in the heart and liver and levels of ER stress markers were all increased in acute iron-loaded rats. N-Acetylcysteine (150 mg/kg, s.c.) lowered the levels of these parameters in acute iron-loaded rats. 4. The results of the present study indicate that ER stress may play an important role in iron-induced tissue injury and that reactive oxygen species may mediate the ER stress response in the pathogenesis of iron-overload cellular injury.
PMID: 19594550 [PubMed - in process]