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Passive smoking reduces and vitamin C increases exercise-induced oxidative stress: does this make passive smoking an anti-oxidant and vitamin C a pro-oxidant stimulus?

Biochemical and biophysical research communications
January 1, 1970
Anastasios A Theodorou et al. (5 authors)
Journal ArticleRandomized Controlled TrialHuman StudyClinical
Study Details

Study Goal

The researchers aimed to compare the effects of chronic passive smoking (pro-oxidant) and vitamin C supplementation (antioxidant) on exercise-induced oxidative stress biomarkers.

Results Summary

Chronic passive smoking increased F2-isoprostanes and decreased glutathione at rest, reducing exercise-induced oxidative stress, while vitamin C supplementation had the opposite effect, increasing oxidative stress post-exercise. The findings challenge the current consensus on antioxidant effects.

Population

20 men randomly assigned to passive smoking or vitamin C groups.

Effective Dosage

Not specified

Duration

12 days

Interactions

None mentioned

Extracted Claims (6)
InterventionDirectionEndpointPopulationDosageImpactClaim #
chronic exposure to passive smoking
increase
level of F2-isoprostanes at rest
twenty men
-
increased
#1
chronic exposure to passive smoking
decrease
level of glutathione at rest
twenty men
-
decreased
#2
chronic exposure to passive smoking
no change
oxidative stress after exercise
twenty men
-
resulted in minimal increase or absence of oxidative stress after exercise
#3
chronic supplementation with vitamin C
decrease
level of F2-isoprostanes at rest
twenty men
-
decreased
#4
chronic supplementation with vitamin C
increase
level of glutathione at rest
twenty men
-
increased
#5
chronic supplementation with vitamin C
increase
exercise-induced oxidative stress
twenty men
-
resulted in marked exercise-induced oxidative stress
#6
Abstract

The current interpretative framework states that, for a certain experimental treatment (usually a chemical substance) to be classified as "anti-oxidant", it must possess the property of reducing (or even nullifying) exercise-induced oxidative stress. The aim of the study was to compare side by side, in the same experimental setup, redox biomarkers responses to an identical acute eccentric exercise session, before and after chronic passive smoking (considered a pro-oxidant stimulus) or vitamin C supplementation (considered an anti-oxidant stimulus). Twenty men were randomly assigned into either passive smoking or vitamin C group. All participants performed two acute eccentric exercise sessions, one before and one after either exposure to passive smoking or vitamin C supplementation for 12 days. Vitamin C, oxidant biomarkers (F2-isoprostanes and protein carbonyls) and the non-enzymatic antioxidant (glutathione) were measured, before and after passive smoking, vitamin C supplementation or exercise. It was found that chronic exposure to passive smoking increased the level of F2-isoprostanes and decreased the level of glutathione at rest, resulting in minimal increase or absence of oxidative stress after exercise. Conversely, chronic supplementation with vitamin C decreased the level of F2-isoprostanes and increased the level of glutathione at rest, resulting in marked exercise-induced oxidative stress. Contrary to the current scientific consensus, our results show that, when a pro-oxidant stimulus is chronically delivered, it is more likely that oxidative stress induced by subsequent exercise is decreased and not increased. Reversely, it is more likely to find greater exercise-induced oxidative stress after previous exposure to an anti-oxidant stimulus. We believe that the proposed framework will be a useful tool to reach more pragmatic explanations of redox biology phenomena.

Medical Subject Headings (MeSH)
AntioxidantsAscorbic AcidBiomarkersCreatine KinaseExerciseF2-IsoprostanesHumansMaleModels, BiologicalMuscle, SkeletalOxidantsOxidation-ReductionOxidative StressRestTobacco Smoke PollutionYoung Adult
Study Links
Quality Scores
SafetyNot Assessed
Efficacy70/10
Quality80/10
Citation Metrics
Total Citations19
Citations/Year1.7
Relative Citation Ratio0.70
NIH Percentile37.2%
Research Impact Scores
APT Score0.25
Weight Score1.73
Normalized Score0.64
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