Near Infrared, High Energy, Ultrashort Pulse Laser-Light Exposure Genetically Induces p53, a Gene in the DNA Repair and Cell Suicide Pathways in Cultured Human Cells

摘要

The use of laser light for targeting devices and weapons has sharply increased the likelihood that aircrew and support personnel will be exposed to laser light during operations. The increased potential for exposure of humans highlights the need for scientifically-based safety standards for laser exposure at the ultrashort pulse lengths. Current safety standards are largely extrapolations of exposure limits at longer pulse lengths using a minimal visible lesion endpoint in the Rhesus monkey retinal model. A non-animal model for assessing laser-light damage to tissue, particularly human, is quite desirous for obvious scientific, political, and fiduciary reasons. We assessed the sublethal insult to human cells using a tissue culture system for specific genes that have been shown to be important in several biological processes that could lead to cancer or cell death. Using the CAT-Tox (L) (Xenometrix, Inc.) assay, it appears that 1064 nm, nanosecond pulses of laser light is sensed and induces several stress response genes, including p53, a gene in the DNA repair and apoptosis (cell suicide) regulatory pathways in a dose dependent fashion. This approach provides insight into a more global methodology for characterizing environmental stressors via genetic profiling.