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.
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.
Mustata
Georgian T
GT
Case Western Reserve University, Department of Pathology, School of Medicine, 2085 Adelbert Rd., Cleveland, OH 44106, USA.
Rosca
Mariana
M
Biemel
Klaus M
KM
Reihl
Oliver
O
Smith
Mark A
MA
Viswanathan
Ashwini
A
Strauch
Christopher
C
Du
Yunpeng
Y
Tang
Jie
J
Kern
Timothy S
TS
Lederer
Markus O
MO
Brownlee
Michael
M
Weiss
Miriam F
MF
Monnier
Vincent M
VM
D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000627:therapeutic use*; D001786:Blood Glucose / Q000378:metabolism; D001835:Body Weight; D028241:Camellia sinensis; D003094:Collagen / Q000737:chemistry / Q000187:drug effects / Q000378:metabolism*; D003432:Cross-Linking Reagents; D003921:Diabetes Mellitus, Experimental / Q000473:pathology / Q000503:physiopathology*; D003928:Diabetic Nephropathies / Q000473:pathology*; D003930:Diabetic Retinopathy / Q000188:drug therapy*; D005247:Feeding Behavior / Q000187:drug effects; D017127:Glycation End Products, Advanced / Q000378:metabolism; D066298:In Vitro Techniques; D008297:Male; D008928:Mitochondria / Q000473:pathology; D010101:Oxygen Consumption / Q000187:drug effects; D008517:Phytotherapy; D051381:Rats; D011917:Rats, Inbred Lew; D013662:Tea; D014810:Vitamin E / Q000627:therapeutic use*
D000975:Antioxidants; D001786:Blood Glucose; D003432:Cross-Linking Reagents; D017127:Glycation End Products, Advanced; D013662:Tea; D014810:Vitamin E; D003094:Collagen; D001205:Ascorbic Acid