Key result
Carvedilol administration (3.125 mg twice daily for 1 week) significantly reduced ROS generation by polymorphonuclear leukocytes from 314 to 185 mV (P<0.025) in normal subjects.
Why the study?
Does carvedilol reduce reactive oxygen species generation and oxidative damage to amino acids in normal subjects?
Does carvedilol reduce reactive oxygen species generation and oxidative damage to amino acids in normal subjects?
p-value: p=<0.025
Carvedilol demonstrates in vivo antioxidant effects by reducing reactive oxygen species generation and oxidative damage to amino acids in normal subjects.
Supports in vivo antioxidant activity in healthy volunteers; leaves open translation to cardiovascular patients or outcomes.
Background —The purpose of this study was to test whether carvedilol has an antioxidant effect in humans in vivo. Methods and Results —We administered 3.125 mg of carvedilol twice daily to normal subjects for 1 week. ROS generation by polymorphonuclear leukocytes and mononuclear cells fell from 314±183.43 and 303±116 mV to 185±157 and 189±63 mV ( P <0.025), respectively. m -Tyrosine fell from 4.24±0.99 to 4.03±0.97 ng/mL ( P =0.01), and o -tyrosine fell from 4.59±1.10 to 4.24±0.99 ng/mL ( P =0.004) in the absence of a change in phenylalanine concentrations. Conclusions —We conclude that carvedilol significantly inhibits ROS generation by leukocytes and oxidative conversion of phenylalanine to m - and o -tyrosine.
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Dandona et al. (2000) studied Normal subjects. Carvedilol vs. Baseline was evaluated on ROS generation by polymorphonuclear leukocytes and mononuclear cells (p=<0.025). Carvedilol administration (3.125 mg twice daily for 1 week) significantly reduced ROS generation by polymorphonuclear leukocytes from 314 to 185 mV (P<0.025) in normal subjects.
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