ArticleInflammation2017
The Influence of α-Tocopherol on Serum Biochemical Markers During Experimentally Induced Pleuritis in Rats Exposed to Dioxin.
Article in Inflammation, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed, 3 citations in OpenAlex.
- Remote Continuous Microinjury-Triggered Cytokines Facilitate Severe Diabetic Foot Ulcer Healing via the Ras/Raf/MEK/ERK Pathway.Journal of inflammation research · 2025Article
- Tibial Cortex Transverse Transport Facilitates Severe Diabetic Foot Wound Healing via HIF-1α-Induced Angiogenesis.Journal of inflammation research · 2024Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Toxicity of dioxins is wide ranging. Amongst the organs, the liver is the most susceptible to damage by dioxins. Damage caused to liver cells results in promoting inflammatory processes. The aim of this work was to evaluate whether high doses of tocopherol will change the inflammatory response, monitored by biochemical indicators, by improving liver function in rats exposed to tetrachlorodibenzo-p-dioxin (TCDD). The study was conducted on a population of female Buffalo rats. The animals were divided into the following groups: Control Group A-representing physiological norms for the studied diagnostic indicators; Control Group B-subjects were administered a 1% ceragenin solution to induce pleuritis; Study Group 1-where rats were administered α-tocopherol acetate for 3 weeks, after which pleuritis was induced; Study Group 2-rats were administered a single dose of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), while 3 weeks later, pleuritis was induced; and Study Group 3-rats were administered a single dose of TCDD and next, were administered α-tocopherol acetate for 3 weeks, followed by pleuritis induction. The results clearly show that administering tocopherol in the course of inflammation causes changes to the distribution and ratio of in the serum protein fractions, including acute phase proteins. The latter proteins are indicative to the improvement in liver function and linked to protein synthesis and stimulation of the antibody-mediated immunity. Moreover, in the course of inflammation caused by exposure of rats to TCDD, tocopherol significantly affected the acute phase protein concentration.
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Registered trials
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