Evidence map›Paper›PMID 33112573›Full record

ArticleAsian Pacific journal of cancer prevention : APJCP2020

Tobacco Smoke Carcinogens Induce DNA Repair Machinery Function Loss: Protection by Carbon Nanotubes.

Anukriti Dhasmana, Anupam Dhasmana, Hobani Yahya H, Abdullah Farasani, Mahmoud Habibullah, Freah L Alshammary, Saif Khan, Shafiul Haque, Mohtashim Lohani

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Asian Pacific journal of cancer prevention : APJCP, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.1field-weighted citation impact, top 54% 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

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. 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

9 authors at 1 institution in 1 country.

Anukriti DhasmanaHimalayan School of Biosciences, Swami Rama Himalayan University, Dehradun (Uttarakhand), India.
Anupam DhasmanaHimalayan School of Biosciences, Swami Rama Himalayan University, Dehradun (Uttarakhand), India.
Hobani Yahya HDean, Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia.
Abdullah FarasaniDepartment of Medical Laboratory Technology, Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia.
Mahmoud HabibullahEmergency Medical Services Department, Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia.
Freah L AlshammaryDepartment of Preventative Dental Sciences, College of Dentistry, Hail University, Hail, Saudi Arabia.
Saif KhanDepartment of Preventative Dental Sciences, College of Dentistry, Hail University, Hail, Saudi Arabia.
Shafiul HaqueResearch and Scientific Studies Unit, Faculty of Nursing and Allied Health Sciences, Jazan University, Jazan, Saudi Arabia.
Mohtashim LohaniEmergency Medical Services Department, Faculty of Applied Medical Sciences, Jazan University, Jazan, Saudi Arabia.
Jazan University · SA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeDNA damage is a continuous process occurring within the cells caused by intrinsic and extrinsic factors, but it gets repaired regularly. If the DNA repair process is faulty, the incidences of damages/mutations can accumulate in cells resulting in cell transformation. It is hypothesized that the negative variations in DNA repair pathways in even at one point viz. genetic, translational or posttranslational stage may fairly be crucial for the beginning and development of carcinogenesis. Therefore, we investigated the potential of tobacco specific nitrosamines (TSNs) related carcinogens to interact with the enzymes involved in DNA repair mechanisms in the current study.

methodsThe derivatives of cigarettes' smoke like NNK and NNAL are very well known and recognized carcinogens. Therefore, almost 120 enzymes playing crucial role in the DNA repair process have been analysed for their reactivity with NNK and NNAL.

resultsThe molecular docking study helped to screen out,  07 possible DNA repair enzyme targets for NNK, and 12for NNAL. Present study revealed the loss of activity of DNA repair enzymes in the presence of NNK and NNAL, and this accumulation may induce the tendency of DNA damage which can lead the transformation of exposed normal cells in to cancerous cells. This study also demonstrated the protective potential of nanoparticles like SWCNTs/MWCNTs against TSN's induced toxicity; here SWCNT against NNK (-17.16 Kcal/Mol) and MWCNT against NNK -17.01 Kcal/Mol were showing maximum binding affinities than the known biomolecular target of NNK 1UGH (Uracil-DNA glycosylase,-7.82Kcal/Mol).

conclusionCNTs can be applied as chemo-preventive agents against environmental and tobacco induced carcinogens owing to their scavenging potential and warrants for in vivo and in vitro experimental validation of the results obtained from the present study.<br />.

Indexed as

DNA RepairCarcinogensDNA DamageDNA Repair EnzymesHumansNanotubes, CarbonProtein Interaction Domains and MotifsTobacco ProductsTobacco Smoke PollutionCarcinogensDNA Repair EnzymesNanotubes, CarbonTobacco Smoke PollutioncancerDNA damageMolecular dockingNNALNNK

Identifiers

PMID33112573
PMCPMC7798159
OpenAlexW3095039702

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

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.