scholarly journals The <i>in Vivo</i> Antioxidant Effects of (&minus;)-Epigallocatechin-3-Gallate Consumption in Healthy Postmenopausal Women Measured by Urinary Excretion of Secondary Lipid Peroxidation Products

2019 ◽  
Vol 10 (01) ◽  
pp. 15-27
Author(s):  
Chelsey Fiecke ◽  
Mindy Kurzer ◽  
Chi Chen ◽  
A. Saari Csallany
1996 ◽  
Vol 126 (3) ◽  
pp. 643-652 ◽  
Author(s):  
Rosemary C. Wander ◽  
Shi-Hua Du ◽  
Sharon O. Ketchum ◽  
Kenneth E. Rowe

2006 ◽  
Vol 27 (7) ◽  
pp. 1398-1403 ◽  
Author(s):  
Kyoung-Ho Lee ◽  
Helmut Bartsch ◽  
Jagadeesan Nair ◽  
Dong-Ho Yoo ◽  
Yun-Chul Hong ◽  
...  

2016 ◽  
Vol 07 (12) ◽  
pp. 1099-1111
Author(s):  
A. Saari Csallany ◽  
Cheryl E. Ainslie-Waldman ◽  
Lindsay R. Young ◽  
Chi Chen ◽  
Mindy S. Kurzer ◽  
...  

Author(s):  
Dontha Sunitha

<p>ABSTRACT<br />To provide an outlook of the various available methods of antioxidant activity. Various available in vitro and in vivo methods are listed and the<br />procedure to perform the method, its mechanism is also explained in brief. 1,1-diphenyl-2-picrylhydrazyl method was found to be used mostly for the<br />in vitro antioxidant activity evaluation purpose while lipid peroxidation was found as mostly used in vivo antioxidant assay. An ethanol was with the<br />highest frequency as a solvent for extraction purpose. Summarized information on the various methods available provides with reliable information<br />to confirm the benefits of antioxidant effects.<br />Keywords: Antioxidant activity, Reactive oxygen species, Free radical, 1,1-diphenyl-2-picrylhydrazyl, Flavonoid.</p>


1999 ◽  
Vol 96 (5) ◽  
pp. 467-474 ◽  
Author(s):  
Florence WONG ◽  
Arieh BOMZON ◽  
Johane ALLARD ◽  
Peter LIU ◽  
Laurence BLENDIS

Systemic arterial vasodilatation has been implicated in the pathogenesis of sodium retention in cirrhosis. Hydrophobic bile acids, which have vasodilatory actions, may be involved. Ursodeoxycholic acid, a hydrophilic bile acid, could potentially decrease systemic arterial vasodilatation, possibly due to its antioxidant effects, and improve sodium handling in cirrhosis. The effects of ursodeoxycholic acid on systemic, renal and forearm haemodynamics, liver function and renal sodium handling were assessed in vasodilated cirrhotic patients with refractory ascites treated with a transjugular intrahepatic porto-systemic shunt (TIPS). Eight cirrhotic patients with refractory ascites without TIPS placement served as controls for the sodium handling effects of ursodeoxycholic acid. From 1 month post TIPS, seven patients were studied before, after 1 month of treatment with ursodeoxycholic acid (15 mg·day-1·kg-1) and at 1 month follow-up. Lipid peroxidation products were used as indices of its antioxidant effects. Ursodeoxycholic acid caused a significant reduction in sodium excretion in both groups (P< 0.05). This, in the post-TIPS patients (urinary sodium excretion: 35±8 mmol/day at 1 month versus 93±21 mmol/day at baseline, P< 0.05), was due to a significant increase in sodium reabsorption proximal to the distal tubule (P< 0.05), without any significant changes in systemic, renal or forearm haemodynamics, or in liver function. No significant change in lipid peroxidation products was observed. We conclude that: (i) in cirrhotic patients with refractory ascites, ursodeoxycholic acid causes sodium retention, (ii) the abnormality in sodium handling in the post-TIPS cirrhotic patients appears to be the result of a direct effect on the proximal nephron, suggesting that factors other than systemic vasodilatation also contribute to sodium retention in cirrhosis, (iii) caution should be exercised in administering ursodeoxycholic acid in cirrhotic patients with ascites.


Blood ◽  
1997 ◽  
Vol 90 (10) ◽  
pp. 3931-3935 ◽  
Author(s):  
Luigi Iuliano ◽  
Domenico Praticò ◽  
Domenico Ferro ◽  
Valerio Pittoni ◽  
Guido Valesini ◽  
...  

Abstract The mechanism leading to the formation of antiphospholipid antibodies (aPL) is still unknown. Because an in vitro study suggested that aPL may derive from pro-oxidant conditions, we sought a relationship between aPL and isoprostanes, indices of lipid peroxidation in vivo. Thirty patients with systemic lupus erythematosus have been studied. Seventeen (56.6%) were positive for aPL because they had lupus anticoagulant and/or high titer of anticardiolipin antibodies (aCL). Plasma levels of tumor necrosis factor (TNF ) and urinary excretion of two isoprostanes, 8-epi-PGF2α and IPF2α -I, free radical catalyzed oxidation products of arachidonic acid, were measured. Patients with systemic lupus erythematosus had higher urinary excretion of 8-epi-PGF2α and IPF2α -I than controls; urinary excretion of the two isoprostanes was highly correlated (Rho = 0.74, P < .0001). Urinary 8-epi-PGF2α was highly correlated with both aCL titer (Rho = 0.70, P < .0001) and TNF (Rho = 0.84, P < .0001), a measure of disease severity. Excretion of this isoprostane was also higher in those patients who exhibited aPL (P < .0001). Comparable correlations were observed with the isoprostane IPF2α -I. No difference of 8-epi-PGF2α was observed between patients with and without previous history of thrombosis. This study, showing the existence of a close association between aPL and increased in vivo lipid peroxidation, supports the hypothesis that these antibodies may result from pro-oxidative conditions and suggests that inflammation may play an important role.


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