The Use of Sphingomyelin to Protect Against UV Induced DNA Damage in Human Keratinocytes

<p>Non melanoma skin cancer (NMSC) is a serious condition caused by chronic ultraviolet (UV) exposure that leads to DNA damage in skin. UV radiation has the potential to lead to DNA damage, which triggers biochemical pathways within a cell. The result is that the cell either undergoes cell cycle arrest, giving the cell time to repair DNA damage, or apoptosis. Sunscreen is the most commonly used treatment for preventing UV induced skin damage, but it involves a number of undesirable and toxic side effects including damaging the dermis, premature aging of skin and underweight child births. This has led to interest in finding safer alternatives to prevent UV damage without the negative side effects of sunscreen. In particular, bovine milk sphingomyelin (SM) is a compound that has the potential to protect against UV damage without any of the dangerous side effects of sunscreen. Here we present the use of SM for UV protection of human keratinocytes (KRTs) to prevent DNA mutations that result from UV exposure. In particular, analysis of the expression of DNA damage biomarkers p21 and p53 was done to determine the potential of SM to prevent DNA damage associated with UV exposure. Both non-SM treated KRTs and KRTs treated with 0.1% SM media 24 hours prior to UV radiation were fixed and IF-stained at 24 hours following 40 mJ/cm² of UV exposure. Significant differences in both p21 and p53 were observed between the SM treated and non-SM treated cells at the UV dosage level (via t-test; p</p>

Name thesis:degree_name

MS in Biomedical Engineering

Discipline thesis:degree_discipline

Biomedical and General Engineering

Year dc:date.available

2015

Author dc:creator

• Campbell, Kevin

Contributors dc:contributor

• Lily Laiho

• Keratinocytes
• p21
• p53
• UV radiation
• sphingomyelin
• skin cancer

Identifier

10.15368/theses.2015.72

OAI identifier oai:identifier

oai:digitalcommons.calpoly.edu:theses-2556