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Title

Link between MnSOD Ala16Val (rs4880) polymorphism and asthma risk is insignificant from sequential meta-analysis
 

Authors

Hazza A. Alhobeira1, Raju K. Mandal2, Saif Khan3, Sajad A. Dar2, Harishankar Mahto4, Mohd Saeed6, Mohd Wahid2, Mohtashim Lohani5, Mahvish Khan6, Shafiul Haque2

 

Affiliation

1Department of Restorative Dentistry, College of Dentistry, University of Ha段l, Ha段l-2440, Saudi Arabia; 2Research and Scientific Studies Unit, College of Nursing & Allied Health Sciences, Jazan University, Jazan-45142, Saudi Arabia; 3Department of Basic Dental and Medical Sciences, College of Dentistry, University of Ha段l, Ha段l-2440, Saudi Arabia; 4Center for Life Sciences, Central University of Jharkhand, Ranchi-835205, Jharkhand, India; 5Department of Emergency Medical Services, College Applied Medical Sciences, Jazan University, Jazan45142, Saudi Arabia; 6Department of Biology, College of Science, University of Ha段l, Ha段l-2440, Saudi Arabia

 

Email

Dr. Hazza A Alhobeira - Email: hazzalshammary@gmail.com; *Corresponding author

 

Article Type

Research Article

 

Date

Received September 12, 2020; Revision September 15, 2020; Accepted September 18, 2020; Published November 30, 2020

 

Abstract

The mitochondrial manganese superoxide dismutase (MnSOD) enzyme protects lungs against oxidative stress by neutralizing the free radical superoxide produced in the respiratory function. This has relevance to asthma. Therefore, it is of interest to describe the potential effect of MnSOD Ala16Val genetic polymorphism to asthma risk. Known data in this context is inconclusive in nature. The possible link between MnSOD Ala16Val polymorphism and asthma is explored using sequence meta-analysis. Data from the pooled analysis of MnSOD Ala16Val polymorphism using five genetic models i.e., allelic (Val vs. Ala: p=0.846; OR=1.033, 95% CI=0.742 to 1.440) is discussed. Homozygous (Val Val vs. Ala Ala: p=0.517; OR=1.307, 95% CI=0.582 to 2.932) and heterozygous (Val Ala vs. Ala Ala: p=0.307; OR=1.138, 95% CI=0.888 to 1.459) data using the described models are documented. Data from the dominant model (Val Val + Val Ala vs. Ala Ala: p=0.301; OR=1.289, 95% CI=0.797 to 2.085) and the recessive model (Val Val vs. Val Ala + Ala Ala: p=0.761; OR=0.924, 95% CI=0.555 to 1.538) analyses for several ethnic subgroups in this context is reported.

 

Keywords

Asthma; genetic model; meta-analysis; MnSOD; polymorphism; susceptibility

 

Citation

Ahobeirai et al. Bioinformation 16(11): 789-800 (2020)

 

Edited by

P Kangueane

 

ISSN

0973-2063

 

Publisher

Biomedical Informatics

 

License

This is an Open Access article which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. This is distributed under the terms of the Creative Commons Attribution License.