ArticleScientific reports2025
Assessment of blood and urine total antioxidant and oxidative status in alcohol and acetone fatal poisonings.
Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
1 citing paper in PubMed.
- Plasma, Urinary, and Salivary Total Redox Status in Critically Ill Patients with Brain Injury and Secondary Organ Failure.Antioxidants (Basel, Switzerland) · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Heavy alcohol consumption is a common cause of fatal poisoning, unlike acetone poisoning, which is very rare. Although oxidative stress plays a crucial role in alcohol and acetone toxicity, no studies compare the total redox status in fatally poisoned individuals. The total antioxidant capacity (TAC), total oxidative status (TOS), and oxidative stress index (OSI) were examined in the blood and urine of patients fatally poisoned with ethanol (n = 21) and acetone (n = 21), along with healthy controls (n = 21). The TAC, TOS, and OSI concentrations were determined by means of colorimetric methods, and the statistical analysis was conducted through non-parametric tests. The blood TAC and TOS were significantly increased in the ethanol- and acetone-intoxicated cadavers as compared to the controls. The blood TAC levels above 55.12 nmol/mg of protein differentiate alcohol- and acetone-intoxicated subjects from the control group with a high sensitivity and specificity. The blood TAC was also positively correlated with the alcohol (r = 0.504), acetone (r = 0.476), and isopropanol blood levels (r = 0.514). However, the TAC, TOS, and OSI in the blood were poorly correlated with the corresponding urine concentrations. The urinary TAC in the ethanol-poisoned subjects was effectively enhanced in comparison to the control and acetone-poisoned subjects. The urinary TAC was also positively associated with the urine alcohol concentration (r = 0.413) and negatively correlated with the acetone (r = - 0.453) and isopropanol urine levels (r = - 0.36). Fatal alcohol and acetone intoxications disrupt the circulating redox status, favoring antioxidant reactions. Differences in the blood and urine redox homeostasis may be due to the organ toxicity of alcohol and acetone.
Indexed as
Identifiers
What Socratic holds
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 Socratic graph.