Evidence map›Paper›PMID 32170816›Full record

ArticleJournal of clinical laboratory analysis2020

Correlation of lipid peroxidation and nitric oxide metabolites, trace elements, and antioxidant enzymes in patients with sickle cell disease.

Charles Antwi-Boasiako, Gifty Boatemaah Dankwah, Robert Aryee, Charles Hayfron-Benjamin, George Aboagye, Andrew D Campbell

Open access · goldAbstract read
In one paragraph

Article in Journal of clinical laboratory analysis, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed, 1 pooled it
1.3field-weighted citation impact, top 20% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed, 1 synthesis or guideline pooled it, 18 citations in OpenAlex.

  1. Pooled it
  2. Crosstalk Between Sickle Cell Disease and Ferroptosis.International journal of molecular sciences · 2025
    Review
  3. Article
  4. Ferroptosis as an emerging target in sickle cell disease.Current research in toxicology · 2024
    Article
  5. Review
  6. Article
  7. Article
  8. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors at 3 institutions in 2 countries.

Charles Antwi-BoasiakoDepartment of Physiology, School of Biomedical and Allied Health Sciences, University of Ghana, Accra, Ghana.
Gifty Boatemaah DankwahDepartment of Physiology, School of Biomedical and Allied Health Sciences, University of Ghana, Accra, Ghana.
Robert AryeeDepartment of Physiology, School of Biomedical and Allied Health Sciences, University of Ghana, Accra, Ghana.ORCID https://orcid.org/0000-0003-3643-4217
Charles Hayfron-BenjaminDepartment of Physiology, School of Biomedical and Allied Health Sciences, University of Ghana, Accra, Ghana.
George AboagyeDepartment of Nutrition and Dietetics, School of Allied Health Sciences, University of Health and Allied Sciences, Ho, Ghana.
Andrew D CampbellCenter for Cancer and Blood Disorders, Children's National Medical Center, George Washington University School of Medicine and Health Sciences, Washington, DC, USA.
University of Ghana · GHChildren's National · USUniversity of Health and Allied Sciences · GH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundLipid peroxidation plays a very important role in sickle cell pathophysiology. The formation of malondialdehyde (MDA) in patients with sickle cell disease (SCD) may lead to endothelial dysfunction. Nitric oxide (NO) is a known vasodilator which plays a role in endothelial function. The current study determined the association between MDA and NO metabolites (NOx), trace elements, and antioxidant enzymes (SOD and CAT) in patients with SCD. The ratio of MDA/NOx was also determined as an index of oxidative stress in the study groups.

methodsThis was a cross-sectional study involving 90 patients with SCD and 50 "healthy" controls. Blood samples (n = 140) were collected from the study groups. The plasma, sera, and red cells were kept at -20°C for biochemical analyses. Hemoglobin (Hb) and NOx levels were determined in the plasma using Labsystem Multiskan MS and Griess reagent system, respectively. Super oxide dismutase (SOD) and catalase (CAT) levels were determined in the red cells using assay kits from Cayman chemicals. Lipid peroxidation biomarker MDA was determined in the sera using the TBARS assay. Levels of iron (Fe), copper (Cu), and zinc (Zn) were also determined in the sera using Variant 240FS. MDA and NOx ratio was computed for the study groups and compared.

resultsLevels of Hb, NOx, SOD, CAT, and Zn were significantly lower in the patients with SCD (P < .001). MDA, Fe, and MDA/ NOx ratio were, however, significantly higher in the patients with SCD (P < .001). There was no significant correlation between MDA and NOx, SOD, CAT, Fe, and Zn in the study groups. MDA, however, correlated positively and significantly with Cu in the HbSS patients with vaso-occlusive crises (VOC). Gender did not affect the levels of oxidative stress markers.

conclusionsFindings from this study suggest a link between lipid peroxidation and Cu in HbSS patients with VOC. Increased MDA/NOx ratio may contribute to sickle cell pathophysiology by promoting oxidative stress.

Indexed as

Lipid PeroxidationAdultAnemia, Sickle CellAntioxidantsBiomarkersCase-Control StudiesCatalaseFemaleHemoglobin, SickleHumansMaleMalondialdehydeNitric OxideOxidative StressSuperoxide DismutaseTrace ElementsAntioxidantsBiomarkersCatalaseHemoglobin, SickleMalondialdehydeNitric OxideSuperoxide DismutaseTrace Elementsendothelial dysfunctionlipid peroxidationnitric oxide metaboliteoxidative stresssickle cell disease

Identifiers

PMID32170816
PMCPMC7370710
OpenAlexW3012144451

What OpenQuestion holds

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Registered trials

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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.