Related Experiment Videos
Bystander effects may modulate ultraviolet A and B radiation-induced delayed mutagenesis
Jostein Dahle1, Olav Kaalhus, Trond Stokke
1Department of Radiation Biology, The Norwegian Radium Hospital, Montebello, 0310 Oslo, Norway. jostein.dahle@labmed.uio.no
Radiation Research
|March 1, 2005
Summary
Ultraviolet radiation causes lasting genomic instability in cells. A bystander effect, potentially involving cell-to-cell communication, significantly increases delayed mutations after UV exposure.
Area of Science:
- Cellular and Molecular Biology
- Radiation Biology
- Genetics
Background:
- Ultraviolet (UV) radiation induces genomic instability in cells, a phenomenon that can persist across generations.
- The precise mechanisms, timing, and UV type-specific induction of these delayed mutations are not fully understood.
Purpose of the Study:
- To investigate the time course, UV type-dependency, and induction mechanisms of delayed mutations following UV irradiation.
- To explore the role of intercellular communication in UV-induced genomic instability.
Main Methods:
- Utilized the hypoxanthine phosphoribosyl transferase (HPRT) mutation assay in V79 Chinese hamster cells exposed to UVA or UVB radiation.
- Employed a selective cell culture method involving aminopterin and 6-thioguanine to quantify delayed HPRT(-) mutations.
- Assessed the impact of gap junction intercellular communication inhibition on mutation frequencies.
Main Results:
- Observed significantly higher frequencies of delayed HPRT(-) mutations compared to previous cloning methods.
- The enhanced mutation frequency suggests a bystander effect, where cells communicate genetic instability.
- Inhibition of gap junctional communication reduced the delayed mutation frequency, supporting its role.
Conclusions:
- A bystander effect contributes to UV-radiation-induced genomic instability.
- Gap junctional intercellular communication is implicated as a partial mediator of this bystander effect.