Journal of Clinical and Diagnostic Research, ISSN - 0973 - 709X

Users Online : 21990

Original article / research
Table of Contents - Year : 2016 | Month : May | Volume : 10 | Issue : 5 | Page : AC06 - AC08

DNA Damage Analysis in Children with Non-syndromic Developmental Delay by Comet Assay AC06-AC08

Surraj Susai, Parkash Chand, Vishnu Bhat Ballambattu, Nandeesha Hanumanthappa, Raveendranath Veeramani

Correspondence
Dr. Surraj Susai,
9, 13th Cross Street, Avvai Nagar, Lawspet, Puducherry-605 008, India.
E-mail: surraj18@gmail.com

Introduction: Majority of the developmental delays in children are non-syndromic and they are believed to have an underlying DNA damage, though not well substantiated. Hence the present study was carried out to find out if there is any increased DNA damage in children with non-syndromic developmental delay by using the comet assay.

Aim: The present case-control study was undertaken to assess the level of DNA damage in children with non syndromic developmental delay and compare the same with that of age and sex matched controls using submarine gel electrophoresis (Comet Assay).

Materials and Methods: The blood from clinically diagnosed children with non syndromic developmental delay and controls were subjected for alkaline version of comet assay Single cell gel electrophoresis using lymphocytes isolated from the peripheral blood. The comets were observed under a bright field microscope; photocaptured and scored using the Image J image quantification software. Comet parameters were compared between the cases and controls and statistical analysis and interpretation of results was done using the statistical software SPSS version 20.

Results: The mean comet tail length in cases and control was 20.77+7.659m and 08.97+4.398m respectively which was statistically significant (p<0.001). Other comet parameters like total comet length and % DNA in tail also showed a statistically significant difference (p < 0.001) between cases and controls.

Conclusion: The current investigation unraveled increased levels of DNA damage in children with non syndromic developmental delay when compared to the controls.