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Concentration Dependent Effect of (−)‐Epicatechin on Na + /K + ‐ATPase and Ca 2+ ‐ATPase Inhibition Induced by Free Radicals in Hypertensive Patients: Comparison with L‐ascorbic Acid
Author(s) -
Kumar Navneet,
Kant Ruchi,
Maurya Pawan Kumar,
Rizvi Syed Ibrahim
Publication year - 2012
Publication title -
phytotherapy research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.019
H-Index - 129
eISSN - 1099-1573
pISSN - 0951-418X
DOI - 10.1002/ptr.4624
Subject(s) - ascorbic acid , antioxidant , oxidative stress , atpase , chemistry , reactive oxygen species , radical , biochemistry , medicine , enzyme , food science
Although the antioxidant properties of flavonoids are well documented, it is still unclear whether these effects are dependent on radical scavenging or iron chelating activities. Oxidative stress, a state of excessive reactive oxygen species (ROS) activity, is associated with vascular disease conditions such as hypertension. Both the anti‐ and pro‐oxidant effects of tea catechins have been implicated in the alterations of cellular functions that determine their chemoprotective and therapeutic potentials in health and diseases. The present study examined the concentration dependent (10 −7 to 10 −4   m ) effects of (−)‐epicatechin and L‐ascorbic acid on Na + /K + ‐ATPase and Ca 2+ ‐ATPase activity in hypertensive patients and normal subjects. L‐ascorbic acid has been used as a positive control to compare the effect of (−)‐epicatechin. A significant ( p  < 0.0001) decrease in the activities of Na + /K + ‐ATPase and Ca 2+ ‐ATPase was observed in hypertensive patients compared with normal subjects. We report that (−)‐epicatechin shows a significant ( p  < 0.001) dose‐dependent protective effect against oxidative stress induced by tert‐butyl hydroperoxide (t‐BHP), which is manisfested as a decrease in the activity of erythrocyte Na + /K + ‐ATPase and Ca 2+ ‐ATPase, in hypertensive patients as well as normal subjects. The effect of L‐ascorbic acid was also significant ( p  < 0.001) and was comparable with that of (−)‐epicatechin. Copyright © 2012 John Wiley & Sons, Ltd.

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