Assessment of DNA Damage Induced by Terrestrial UV Irradiation of Dried Bloodstains: Forensic Implications

• NCJ Number: 246738
• Journal: Forensic Science International: Genetics Volume: 8 Issue: 1 Dated: January 2014 Pages: 36-43
• Author(s): Ashley Hall; Lynn M. Sims; Jack Ballantyne
• Date Published: January 2014
• Length: 8 pages
• Grant Number(s): 2002-IJ-CX-K001
• Sponsoring Agency: National Institute of Justice (NIJ)
• Publication Format: Article
• Publication Type: Report (Study/Research)
• Language: English
• Country: United States of America

Annotation

Few publications have detailed the nature of DNA damage in contemporary i.e. non-ancient dried biological stains.

Abstract

Few publications have detailed the nature of DNA damage in contemporary i.e. non-ancient dried biological stains. The chief concern, from a forensic standpoint, is that the damage can inhibit polymerase-mediated primer extension, ultimately resulting in DNA typing failure. In the work described here, we analyzed the effects of UVA and UVB irradiation on cell-free solubilized DNA, cell-free dehydrated DNA and dehydrated cellular DNA from bloodstains. After UV exposure ranging from 25 J cm-2 to 1236 J cm-2, we assayed for the presence of bipyrimidine photoproducts BPPPs, oxidative lesions and strand breaks, correlating the damage with the inhibition of STR profiling. Subsequent to irradiation with either UVA and UVB, the incidence of BPPPs, oxidative products and strand breaks were observed in decreasing quantities as follows: cell-free solubilized DNA>cell-free dehydrated DNA>bloodstain DNA. UVA irradiation did not result in even the partial loss of a STR profile in any sample tested. Somewhat different results were observed after genetic analysis of UVB exposed samples, in that the ability to produce a complete STR profile was affected earliest in bloodstain DNA, next in cell-free solubilized DNA and not at all in cell-free dehydrated DNA. Therefore, it is likely that other types of damage contributed to allele-drop-out in these samples but remained undetected by our assays, whereby the endonucleases did not react with the lesions or the presence of the lesions was masked by strand breaks. Under the conditions of the study, strand breaks appeared to be the predominant types of damage that ultimately resulted in DNA typing failure from physiological stains, although some evidence suggested oxidative damage may have played a role as well.