ArticlePloS one2018
Location-dependent effects of trauma on oxidative stress in humans.
Article in PloS one, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 7 citations in OpenAlex.
- Plasma, Urinary, and Salivary Total Redox Status in Critically Ill Patients with Brain Injury and Secondary Organ Failure.Antioxidants (Basel, Switzerland) · 2026Article
- Total Antioxidant Status in Critically Ill Patients with Traumatic Brain Injury and Secondary Organ Failure-A Systematic Review.Diagnostics (Basel, Switzerland) · 2024Review
- Use of Melatonin/Decorticotomy and Autogenous Bone Graft in Induced 1-Wall Defect.International dental journal · 2023Article
- Oxidant/Antioxidant Status Is Impaired in Sepsis and Is Related to Anti-Apoptotic, Inflammatory, and Innate Immunity Alterations.Antioxidants (Basel, Switzerland) · 2022Article
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Though circulating antioxidant capacity in plasma is homeostatically regulated, it is not known whether acute stressors (i.e. trauma) affecting different anatomical locations could have quantitatively different impacts. For this reason, we evaluated the relationship between the anatomical location of trauma and plasma total antioxidant capacity (TAC) in a prospective study, where the anatomical locations of trauma in polytraumatic patients (n = 66) were categorized as primary affecting the brain -traumatic brain injury (TBI)-, thorax, abdomen and pelvis or extremities. We measured the following: plasma TAC by 2 independent methods, the contribution of selected antioxidant molecules (uric acid, bilirubin and albumin) to these values and changes after 1 week of progression. Surprisingly, TBI lowered TAC (919 ± 335 μM Trolox equivalents (TE)) in comparison with other groups (thoracic trauma 1187 ± 270 μM TE; extremities 1025 ± 276 μM TE; p = 0.004). The latter 2 presented higher hypoxia (PaO2/FiO2 272 ± 87 mmHg) and hemodynamic instability (inotrope use required in 54.5%) as well. Temporal changes in TAC are also dependent on anatomical location, as thoracic and extremity trauma patients' TAC values decreased (1187 ± 270 to 1045 ± 263 μM TE; 1025 ± 276 to 918 ± 331 μM TE) after 1 week (p < 0.01), while in TBI these values increased (919 ± 335 to 961 ± 465 μM TE). Our results show that the response of plasma antioxidant capacity in trauma patients is strongly dependent on time after trauma and location, with TBI failing to induce such a response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.