The free oxygen radical scavenging enzymes and redox status in roots and leaves of Populus x Euramericana in response to osmotic stress, desiccation and rehydration

Purpose: To assess associations between a free oxygen radical test (FORT), free oxygen radical defense test (FORD), oxidative stress index, urinary cortisol, countermovement jump (CMJ), and subjective wellness in American college football. Methods: Twenty-three male student athlete American college football players were assessed over 10 weeks: off-season conditioning (3 wk), preseason camp (4 wk), and in season (3 wk). Assessments included a once-weekly FORT and FORD blood sample, urinary cortisol sample, CMJ assessment including flight time, reactive strength index modified and concentric impulse, and a daily subjective wellness questionnaire. Linear mixed models analyzed the effect of a 2 within-subject SD change in the predictor variable on the dependent variable. The effects were interpreted using magnitude-based inference and are presented as standardized effect size (ES) ± 90% confidence intervals. Results: Small negative associations were observed between FORT–flight time, FORT–fatigue, FORT–soreness (ES range = −0.30 to −0.48), FORD–sleep (ES = 0.42 ± 0.29), and oxidative stress index soreness (ES = 0.56 ± 0.29). Small positive associations were observed between FORT–cortisol (ES = 0.36 ± 0.35), FORD–flight time, FORD reactive strength index modified and FORD–soreness (0.37–0.41), oxidative stress index concentric impulse (ES = 0.37 ± 0.28), and with soreness–concentric impulse, soreness–flight time, and soreness reactive strength index modified (0.33–0.59). Moderate positive associations were observed between cortisol–concentric impulse and cortisol–sleep (0.57–0.60). Conclusion: FORT/FORD was associated with CMJ variables and subjective wellness. Greater amounts of subjective soreness were associated with decreased CMJ performance, increased FORT and cortisol, and decreased FORD.

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Purine nucleoside phosphorylase: A new marker for free oxygen radical injury to the endothelial cell

Hepatology ◽

10.1002/hep.1840110206 ◽

1990 ◽

Vol 11 (2) ◽

pp. 193-198 ◽

Cited By ~ 62

Author(s):

Prakash N. Rao ◽

Thomas R. Walsh ◽

Leonard Makowka ◽

Randy S. Rubin ◽

Thomas Weber ◽

...

Keyword(s):

Endothelial Cell ◽

Purine Nucleoside Phosphorylase ◽

Oxygen Radical ◽

Purine Nucleoside ◽

Free Oxygen Radical ◽

Free Oxygen ◽

Nucleoside Phosphorylase

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ABSTRACT

PEDIATRICS ◽

10.1542/peds.97.6.870 ◽

1996 ◽

Vol 97 (6) ◽

pp. 870-870

Keyword(s):

Free Radicals ◽

Intestinal Bacteria ◽

Oxygen Radical ◽

Oral Iron ◽

Oxygen Scavengers ◽

Free Oxygen Radical ◽

Free Oxygen ◽

Malnourished Children ◽

Iron Deficient ◽

Low Levels

This article addresses the unsettled controversy about the use of iron in the treatment of children with malnutrition. Although many malnourished children are iron-deficient, there are at least two reasons why oral iron may be detrimental: 1) low levels of transferrin are common in such children which decreases the absorption of oral iron, thus promoting the growth of intestinal bacteria; and 2) iron that is absorbed, but which remains unbound, is converted from the ferrous to the ferric state and becomes an aggressive and potentially damaging free oxygen radical. The authors used the bleomycin assay to quantify the free or loosely bound iron in 50 children with kwashiorkor and compared this data with that found in six children with marasmus and 12 well-nourished children. Nonprotein-bound iron was found in 58% of the children with kwashiorkor, but in none of the others. Many children who are malnourished are deficient in micronutrients, such as vitamins A and E, zinc, and glutathione, which serve as free oxygen scavengers. An imbalance in free radicals and their scavengers results in tissue damage and potentially increases the morbidity and mortality in these precarious children. If the finding of these investigators is substantiated, it will add credence to the argument advising caution in respect to oral iron therapy in children with kwashiorkor.

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Sequestration and Oxygen Radical Detoxification as Mechanisms of Paraquat Resistance

Weed Science ◽

10.1017/s0043174500080395 ◽

1994 ◽

Vol 42 (2) ◽

pp. 277-284 ◽

Cited By ~ 36

Author(s):

Jonathan J. Hart ◽

Joseph M. Di Tomaso

Keyword(s):

Active Oxygen Species ◽

Radical Scavenging ◽

Resistance Mechanisms ◽

Oxygen Radical ◽

Membrane Properties ◽

Chloroplast Envelope ◽

Cross Resistance ◽

Paraquat Resistance ◽

Plant Cell Membranes ◽

Scavenging Enzymes

Evidence in the literature has generally supported either of two paraquat resistance mechanisms: an increase in activity of oxygen radical-scavenging enzymes in resistant plants which affords protection from active oxygen species formed by paraquat; and sequestration of paraquat away from its site of action in the chloroplast. Evidence for the first model relies primarily on measurement of increased enzyme activity and cross-resistance to other oxygen radical-generating stresses in resistant plants. The sequestration model is supported by data showing decreased translocation of paraquat and absence of paraquat injury in plant systems that do not have increased levels of protective enzymes. An alteration in paraquat transport at one of several plant cell membranes could confer resistance by modifying movement of paraquat into the compartment bounded by that membrane. Properties of the plasmalemma, chloroplast envelope, and tonoplast that may be important to paraquat transport are discussed and data supporting or discounting specific membrane alterations in resistant plants are presented. Finally, the possibility that both mechanisms may work in concert is addressed.

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