11 replies to this topic

[opales]

The total mortality lowering effects of green tea aside, I have never seen this side of the coin discussed anywhere. The notion of changing balance from oxidative to carbonyl stress appears interesting (and frightning).

Paradoxical Effects of Green Tea (Camellia Sinensis) and Antioxidant Vitamins in Diabetic Rats

Improved Retinopathy and Renal Mitochondrial Defects but Deterioration of Collagen Matrix Glycoxidation and Cross-Linking
Georgian T. Mustata1, Mariana Rosca2, Klaus M. Biemel3, Oliver Reihl3, Mark A. Smith1, Ashwini Viswanathan1, Christopher Strauch1, Yunpeng Du2, Jie Tang2, Timothy S. Kern2, Markus O. Lederer3,{dagger}, Michael Brownlee4, Miriam F. Weiss2, and Vincent M. Monnier1,5

1 Department of Pathology, School of Medicine, Case Western Reserve University, Cleveland, Ohio
2 Department of Medicine, School of Medicine, Case Western Reserve University, Cleveland, Ohio
3 Institut für Lebensmittelchemie, Universität Hohenheim, Stuttgart, Germany
4 Albert Einstein College of Medicine, Bronx, New York
5 Department of Biochemistry, School of Medicine, Case Western Reserve University, Cleveland, Ohio

We tested the hypothesis that green tea prevents diabetes-related tissue dysfunctions attributable to oxidation. Diabetic rats were treated daily with tap water, vitamins C and E, or fresh Japanese green tea extract. After 12 months, body weights were decreased, whereas glycated lysine in aorta, tendon, and plasma were increased by diabetes (P < 0.001) but unaffected by treatment. Erythrocyte glutathione and plasma hydroperoxides were improved by the vitamins (P < 0.05) and green tea (P < 0.001). Retinal superoxide production, acellular capillaries, and pericyte ghosts were increased by diabetes (P < 0.001) and improved by green tea and the vitamins (P variable). Lens crystallin fluorescence at 370/440 nm was ameliorated by green tea (P < 0.05) but not the vitamins. Marginal effects on nephropathy parameters were noted. However, suppressed renal mitochondrial NADH-linked ADP-dependent and dinitrophenol-dependent respiration and complex III activity were improved by green tea (P variable). Green tea also suppressed the methylglyoxal hydroimidazolone immunostaining of a 28-kDa mitochondrial protein. Surprising, glycoxidation in tendon, aorta, and plasma was either worsened or not significantly improved by the vitamins and green tea. Glucosepane cross-links were increased by diabetes (P < 0.001), and green tea worsened total cross-linking. In conclusion, green tea and antioxidant vitamins improved several diabetes-related cellular dysfunctions but worsened matrix glycoxidation in selected tissues, suggesting that antioxidant treatment tilts the balance from oxidative to carbonyl stress in the extracellular compartment.

Address correspondence and reprint requests to Vincent M. Monnier, Case Western Reserve University, Department of Pathology, School of Medicine, 2085 Adelbert Rd., Cleveland, OH 44106. E-mail: vmm3@po.cwru.edu

[biknut]

Time and time again we see studies that show taking vitamin C and E have negative effects or no positive effects.

I think instead of changing the balance it's more likely this result was because of more oxidative stress caused by the vitamin C and E.

[health_nutty]

Thanks for the post opales. Maybe this points to an increased need of AGE inhibitors/breakers if on high doses of antioxidants. I wonder if the effect is dosage related as rat studies tend to use extremely high doses.

[xanadu]

biknut, I'd like to see something to back up your statement about C and E having negative effects. You have been reading too many propaganda pieces by the pharmaceutical industry. You and opales both.

All this study showed is that green tea is not an AGE inhibitor. So what? It does enough good things on it's own and has been shown to reduce morbidity and increace lifespan. Take green tea for what it does and take benfotiamine and other things for what they do.

[opales]

All this study showed is that green tea is not an AGE inhibitor. So what?

No, "green tea increased total crosslinking" and "in conclusion... green tea and vitamins...worsened matrix glycoxidation in selected tissues". These are explicitly stated in the abstract.

Some studies have found increased mortality from vitamin E (alpha tocopherol form), and in general supplemental C and E do not increase total mortality or reduce death from major killers, despite initial promise. Here is a potential explanation (in addition to those stated before).

[Athanasios]

There are quite a few studies showing that green tea inhibits AGE. It may be the Vit C and E (amount and/or form) causing the effects. Are there other studies that come to the same conclusion. Wish I had more time, but I will look up more stuff later.

[health_nutty]

" There are quite a few studies showing that green tea inhibits AGE"

Can you point me to those studies? I'd be very interesting in reading them.

BTW, thanks for the bentotiamine info. It was a great read.

ps, hope your finals went well. (I'm soooo glad I'm done with finals for good).

[Athanasios]

I only entered "green tea glycation" into pubmed.nl

you can do further searches by doing just "tea glycation" "green tea AGE" and other similar terms and combonations to get more.

thanks, finals went well....catching up on chores and sleep now!

[health_nutty]

I only entered "green tea glycation" into pubmed.nl

you can do further searches by doing just "tea glycation" "green tea AGE" and other similar terms and combonations to get more.

thanks, finals went well....catching up on chores and sleep now!

Thanks again.

[biknut]

biknut, I'd like to see something to back up your statement about C and E having negative effects.

This was a recent one posted on this forum. I've seen a great many more. What I've found very hard to find is a study that showed where vitamin C or E actually reduced oxidative stress.


Life-long vitamin C supplementation in combination with cold exposure does not affect oxidative damage or lifespan in mice, but decreases expression of antioxidant protection genes.Selman C, McLaren JS, Meyer C, Duncan JS, Redman P, Collins AR, Duthie GG, Speakman JR.
Aberdeen Centre for Energy Regulation and Obesity (ACERO), School of Biological Sciences, University of Aberdeen, Aberdeen AB24 2TZ, UK.

Oxidative stress is suggested to be central to the ageing process, with endogenous antioxidant defence and repair mechanisms in place to minimize damage. Theoretically, supplementation with exogenous antioxidants might support the endogenous antioxidant system, thereby reducing oxidative damage, ageing-related functional decline and prolonging life- and health-span. Yet supplementation trials with antioxidants in animal models have had minimal success. Human epidemiological data are similarly unimpressive, leading some to question whether vitamin C, for example, might have pro-oxidant properties in vivo. We supplemented cold exposed (7+/-2 degrees C) female C57BL/6 mice over their lifespan with vitamin C (ascorbyl-2-polyphosphate), widely advocated and self administered to reduce oxidative stress, retard ageing and increase healthy lifespan. No effect on mean or maximum lifespan following vitamin C treatment or any significant impact on body mass, or on parameters of energy metabolism was observed. Moreover, no differences in hepatocyte and lymphocyte DNA oxidative damage or hepatic lipid peroxidation was seen between supplemented and control mice. Using a DNA macroarray specific for oxidative stress-related genes, we found that after 18 months of supplementation, mice exhibited a significantly reduced expression of several genes in the liver linked to free-radical scavenging, including Mn-superoxide dismutase. We confirmed these effects by Northern blotting and found additional down-regulation of glutathione peroxidase (not present on macroarray) in the vitamin C treated group. We suggest that high dietary doses of vitamin C are ineffective at prolonging lifespan in mice because any positive benefits derived as an antioxidant are offset by compensatory reductions in endogenous protection mechanisms, leading to no net reduction in accumulated oxidative damage.

[chipdouglas]

It can get very confusing--some study comes out saying vitamin benefical for issue A and there comes yet another disproving it etc.......I'm sure you'all get my drift.

[health_nutty]

There are quite a few studies showing that green tea inhibits AGE. It may be the Vit C and E (amount and/or form) causing the effects. Are there other studies that come to the same conclusion. Wish I had more time, but I will look up more stuff later.

All the studies I could find on pubmed had the opposite conclusion. Here are just a few:

http://www.ncbi.nlm....l=pubmed_docsum

Green tea extract suppresses the age-related increase in collagen crosslinking and fluorescent products in C57BL/6 mice.

* Rutter K,
* Sell DR,
* Fraser N,
* Obrenovich M,
* Zito M,
* Starke-Reed P,
* Monnier VM.

Yorktown High School, Arlington, VA 22207, USA.

Collagen crosslinking during aging in part results from Maillard reaction endproducts of glucose and oxoaldehydes. Because of the tight link between oxidative and carbonyl stress, we hypothesized that natural antioxidants and "nutriceuticals" could block collagen aging in C57BL/6 mice. Six groups of young and adult mice received vitamin C, vitamin E, vitamin C&E, blueberry, green tea extract (GTE), or no treatment for a period of 14 weeks. Body weights and collagen glycation were unaltered by the treatment. However, GTE or vitamin C&E combined blocked tendon crosslinking at 10 months of age (p < 0.05, adult group). GTE also blocked fluorescent products at 385 and 440 nm (p = 0.052 and < 0.05, respectively) and tended to decrease skin pentosidine levels. These results suggest that green tea is able to delay collagen aging by an antioxidant mechanism that is in part duplicated by the combination of vitamin C and E.

PMID: 14743550 [PubMed - indexed for MEDLINE]


http://www.ncbi.nlm....l=pubmed_docsum

Therapeutic effect of green tea extract on advanced glycation and cross-linking of collagen in the aorta of streptozotocin diabetic rats.

* Babu PV,
* Sabitha KE,
* Shyamaladevi CS.

Department of Biochemistry, University of Madras, Guindy Campus, Chennai, India.

1. The therapeutic effect of green tea extract (GTE) on the aortic collagen content and its characteristics were investigated in streptozotocin diabetic rats. 2. Diabetes was induced in rats by a single intra peritoneal injection of streptozotocin (60 mg/kg bodyweight). Six weeks after diabetes induction, GTE was administered orally for four weeks (300 mg/kg bodyweight daily). Systolic blood pressure, blood glucose, anti-oxidant status, collagen content, extent of glycation, collagen linked fluorescence and aortic collagen solubility pattern were determined in experimental rats. 3. At the end of the experimental period, there was a significant increase in the systolic blood pressure and blood glucose in diabetic rats. The lipid peroxides increased whereas glutathione and vitamin C levels were decreased in the serum of diabetic rats. The collagen content, extent of glycation, the advanced glycation end products (AGEs) and degree of cross-linking were increased in the aorta of diabetic rats. 4. The oral administration of GTE to diabetic rats significantly reduced the systolic blood pressure and blood glucose. The level of lipid peroxides reduced and the content of glutathione and vitamin C increased in the serum of GTE treated diabetic rats. Green tea extract also impede the accumulation of aortic collagen, extent of glycation, formation of AGEs and cross-linking of collagen in diabetic rats. The antihyperglycemic, anti-oxidant and antiglycating effects of GTE ascribed for these beneficial effects. In conclusion, green tea may have therapeutic effect in the treatment of cardiovascular complications characterized by increased AGE accumulation and protein cross-linking associated with diabetes.

Trapping reactions of reactive carbonyl species with tea polyphenols in simulated physiological conditions.

* Lo CY,
* Li S,
* Tan D,
* Pan MH,
* Sang S,
* Ho CT.

Department of Food Science, Rutgers University, New Brunswick, NJ, USA. Fax: +1-732-932-6776.




http://www.ncbi.nlm....l=pubmed_docsum

Trapping reactions of reactive carbonyl species with tea polyphenols in simulated physiological conditions.

The carbonyl stress that leads to the formation of advanced glycation end products (AGEs) in diabetes mellitus has drawn much attention recently. Reactive alpha-dicarbonyl compounds, such as glyoxal (GO) and methylglyoxal (MGO), have been shown to be a high potential glycation agent in vitro and in vivo. In this study, epicatechins in green tea and theaflavins in black tea were found to be able to reduce the concentration of MGO in physiological phosphate buffer conditions. Modified MGO derivatization for GC/flame ionization detector (FID) method in quantification was systematically conducted. In molar ratio of 3 (MGO/polyphenol), theaflavin-3,3'-digallate (TF3) in theaflavins and (-)-epigallocatechin (EGC) in epicatechins showed the highest MGO reduction at 66.65 and 45.74%, respectively, after 1 h of incubation. In kinetic study (molar ratio of MGO/polyphenol = 1:1), rapid MGO reduction occurred within 10 min. Identities of primary adducts between (-)-epigallocatechin gallate (EGCG) and MGO were determined. Newly generated stereoisomers at the C8 position of EGCG A-ring were isolated with a chiral column, and structurally confirmed by 2-D NMR analyses.

PMID: 17103374 [PubMed - as supplied by publisher]