Evidence map›Paper›PMID 22752389›Full record

ArticleMolecular and cellular biochemistry2012

Selenium as a modulator of membrane stability parameters and surface changes during the initiation phase of 1,2-dimethylhydrazine induced colorectal carcinogenesis.

Fereshteh Ezzati Ghadi, Anshoo Malhotra, Abdollah Ramzani Ghara, D K Dhawan

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Article in Molecular and cellular biochemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing papers in PubMed
0.9field-weighted citation impact, top 25% 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

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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

4 citing papers in PubMed, 11 citations in OpenAlex.

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4 · The record

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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

4 authors at 1 institution in 1 country.

Fereshteh Ezzati GhadiDepartment of Biophysics, Panjab University, Chandigarh, India.
Anshoo Malhotra
Abdollah Ramzani Ghara
D K Dhawan
Panjab University · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The present study evaluated the modulatory potential of selenium on colonic surface abnormalities and membrane fluidity changes following 1,2-dimethylhydrazine (DMH) induced colon carcinogenesis. Rats were segregated into four groups viz., normal control, DMH treated, selenium treated, and DMH + selenium treated. Initiation of molecular events leading to colon carcinogenesis was started following weekly subcutaneous injections of DMH (30 mg/Kg body weight) for 10 weeks. Selenium in the form of sodium selenite was supplemented to rats at a dose level of 1 PPM in drinking water, ad libitum for the entire duration of the study. Brush border membranes were isolated from the colon of rats and the viscosity as well as fluidity parameters were assessed using the membrane extrinsic fluorophore pyrene. DMH treatment resulted in a significant increase in lipid peroxidation. Reduced glutathione levels (GSH) and the activities of glutathione reductase (GR), glutathione transferase (GST), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GPx) were found to be significantly decreased following DMH treatment. On the other hand, supplementation with selenium to DMH treated rats resulted in a significant decrease in the levels of lipid peroxidation but caused a significant increase in the levels of GSH as well in the activities of GR, GST, SOD, CAT, and GPx. The results further, demonstrated a marked decrease in membrane microviscosity following DMH treatment. On the other hand, a significant increase was observed in the excimer/monomer ratio and fluidity parameter of DMH treated rats when compared to normal control rats. However, the alterations in membrane microviscosity and the fluidity parameters were significantly restored following selenium treatment. Further, histological as well as colon surface alterations were also observed following DMH treatment, which however were greatly prevented upon selenium co-administration. The study, therefore, concludes that selenium proves as a useful in modulating the colonic surface abnormalities and membrane stability following DMH induced colon carcinogenesis.

Indexed as

Colorectal Neoplasms1,2-DimethylhydrazineAnimalsAnticarcinogenic AgentsAntioxidantsCarcinogensCatalaseCell Membrane StructuresCell Transformation, NeoplasticGlutathioneGlutathione PeroxidaseGlutathione ReductaseGlutathione TransferaseLipid PeroxidationMaleMicrovilli1,2-DimethylhydrazineAnticarcinogenic AgentsAntioxidantsCarcinogensCatalaseGlutathioneGlutathione PeroxidaseGlutathione ReductaseGlutathione TransferaseSodium SeleniteSuperoxide Dismutase

Identifiers

PMID22752389
OpenAlexW2079290420

What OpenQuestion holds

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Read underepoch 390

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.