DNA damage and integrity of UV-induced DNA repair in lymphocytes of smokers analysed by the comet assay

• Published in: Mutation research Vol. 520; no. 1; pp. 179 - 187
• Main Authors: Mohankumar, Mary N, Janani, S, Prabhu, B.Karthikeya, Kumar, P.R.Vivek, Jeevanram, R.K
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 26.09.2002; Elsevier
• Subjects: Adult; Biological and medical sciences; Case-Control Studies; Comet assay; Comet Assay - methods; DNA Damage - drug effects; DNA repair; DNA Repair - genetics; DNA Repair - radiation effects; DNA, Single-Stranded - drug effects; DNA, Single-Stranded - radiation effects; Fundamental and applied biological sciences. Psychology; Genetic polymorphism; Humans; Inter-individual variability; Kinetics; Lymphocytes - drug effects; Lymphocytes - radiation effects; Middle Aged; Molecular and cellular biology; Molecular genetics; Mutagenesis. Repair; Nucleotide excision repair (NER); Single cell gel electrophoresis; Smokers; Smoking - adverse effects; Ultraviolet Rays - adverse effects; UV-induced DNA damage; Smokers; Single cell gel electrophoresis; Inter-individual variability; UV-induced DNA damage; Genetic polymorphism; DNA repair; Comet assay; Nucleotide excision repair (NER); Repair; Smoker; Lymphocyte; DNA; Integrity
• ISSN: 1383-5718; 0027-5107; 1879-3592
• DOI: 10.1016/S1383-5718(02)00201-2

DNA damage was assessed in smoker lymphocytes by subjecting them to the single cell gel electrophoresis (SCGE) assay. In addition to the appearance of comet tails, smoker cells exhibited enlarged nuclei when analysed by the comet assay. On comparing basal DNA damage among smokers and a non-smoking control group, smoker lymphocytes showed higher basal DNA damage (smokers, 36.25±8.45 μm; non-smokers, 21.6±2.06 μm). A significant difference in DNA migration lengths was observed between the two groups at 10 min after UV exposure (smokers, 65.5±20.34 μm; non-smokers, 79.2±11.59 μm), but no significant differences were seen at 30 min after UV exposure (smokers, 21.13±10.73 μm; non-smokers, (27.2±4.13 μm). The study thus implies that cigarette smoking perhaps interferes with the incision steps of the nucleotide excision repair (NER) process. There appeared be no correlation between the frequency of smoking and DNA damage or the capacity of the cells to repair UV-induced DNA damage that suggests inherited host factors may be responsible for the inter-individual differences in DNA repair capacities. The study also suggests monitoring NER following UV insult using the SCGE assay is a sensitive and simple method to assess DNA damage and integrity of DNA repair in human cells exposed to chemical mutagens.