I can't figure out what Vitasearch is saying here.
Quote:
In a study involving 36 elderly patients with type 2 diabetes, administration of vitamin C was found to significantly increase cellular reduced glutathione levels, vitamin C levels, and vitamin E content of LDL?http://www.vitasearch.com/get-clp-summary/37159
What does "significantly increase cellular reduced" mean, and do they mean increased reduced Vit C & Vit E?
I guess my senile mind must be increasingly reduced, my mind, not the senility.
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For now we see through a glass, darkly.... 1st Corinthians 13:12
Iggy, I think they need to re-write it. It doesn't make sense as it is.
If they are talking about reduced-glutathione in cells, they could find a clearer way of saying so.
Is there a way to e-mail them, to ask for clarification?
I can't figure out what Vitasearch is saying here.
What does "significantly increase cellular reduced" mean, and do they mean increased reduced Vit C & Vit E?
I guess my senile mind must be increasingly reduced, my mind, not the senility.
I think what they are saying is that the levels are reduced before introduction of vitamin C. but, I admit, the sentence is very confusing. A lot of these abstracts are not clear. sometimes scientists are not the best writers.
the email is in the report. I bet if you emailed them, they would explain. I have found most researchers will explain if you write them. I think they want people to understand their research.
Yes, that's my understanding. Here's the full abstract:
Quote:
In a study involving 36 elderly patients with type 2 diabetes, administration of vitamin C was found to significantly increase cellular reduced glutathione levels, vitamin C levels, and vitamin E content of LDL.
Patients were randomized into 3 groups: Group 1 received 0.5 g/d vitamin C; Group 2 received 1 g/d vitamin C, and Group 3 received a placebo.
Compared to subjects in the placebo group, those in the 0.5 g/d and 1 g/d vitamin C groups experienced significant increases in cellular reduced glutathione levels (0.60 and 0.93, respectively, compared with 0.33 in the placebo group).
Subjects in the 1 g/d vitamin C group also experienced significant increases in vitamin C (5.66 vs 2.72) and in vitamin E content of LDL (1.98 vs 1.48). No significant changes in lipid peroxidation markers or susceptibility of LDL to peroxidation provoked by gamma-radiolysis were observed.
These results suggest that, "…Vit-C has a dose-dependent effect on the cellular contents of antioxidants and on vitamin E content of LDL in elderly patients with type 2 DM." However, the authors conclude, "These changes are not sufficient to decrease the LDL susceptibility to peroxidation."
Quote:
Increased lipid peroxidation due to an altered intracellular ratio between free radicals and antioxidant systems has been associated with development of diabetic complications. This report explores the biochemical reliability of this hypothesis by measuring glutathione (GSH) in overweight patients with poorly controlled type 2 diabetes. GSH, a crucial antioxidant and cofactor for the selenium-dependent glutathione peroxidase (GSHPx), was analyzed in red blood cells.
Ten overweight and poorly controlled type 2 diabetic patients (6 women and 4 men, age 45 -60 years, body mass index (BMI) 26 -32 kg/m2, HbA1c > 9.4%) and 13 healthy normal weight controls (7 women and 6 men, age 40-60 years, BMI 20-25 kg/m2, HbA1c <6.0 %) were included in the study.
The intracellular level of GSH in red blood cells (mean 1.54 mmol/l) of the diabetic patients was reduced to 60% of reference values (mean 2-6 mmol/l). Reduced activity of GSHPx and increased levels of peroxides in diabetic patients have been found previously.
Discussed are several mechanisms that contribute to the depletion of GSH in poorly controlled type 2 diabetic patients, involving reduced levels of NADPH that is essential for the regeneration of GSH in vivo. The probability of direct trapping of GSH to sugar aldehydes that invade the intracellular space in diabetic states should also be taken into account.
Therapeutic trials with antioxidants that can regenerate the intracellular level of GSH are scarce but promising. An attractive hypothesis is that intracellular excesses of glucose inhibit the antioxidant systems primarily by its ability to cause depletion of the crucial protector GSH. The ultimate effects of such derangement of the protective systems against free radicals may involve vascular and neurological complications. J. Trace Elem. Exp. Med. 13:105-111, 2000.