Bacterial inactivation by solar ultraviolet radiation compared with sensitivity to 254 nm radiation.

Our goal was to derive a quantitative factor that would allow us to predict the solar sensitivity of vegetative bacterial cells to natural solar radiation from the wealth of data collected for cells exposed to UVC (254 nm) radiation. We constructed a solar effectiveness spectrum for inactivation of vegetative bacterial cells by combining the available action spectra for vegetative cell killing in the solar range with the natural sunlight spectrum that reaches the ground. We then analyzed previous studies reporting the effects of solar radiation on vegetative bacterial cells and on bacterial spores.

Overview of the inactivation by 254 nm ultraviolet radiation of bacteria with particular relevance to biodefense.

Our goal was to ultimately predict the sensitivity of untested bacteria (including those of biodefense interest) to ultraviolet (UV) radiation. In this study, we present an overview and analysis of the relevant 254 nm data previously reported and available in the literature. The amount of variability in this data prevented us from determining an "average" response for any bacterium.

Action spectra again?

Action spectroscopy has a long history and is of central importance to photobiological studies. Action spectra were among the first assays to point to chlorophyll as the molecule most responsible for plant growth and to DNA as the genetic material. It is useful to construct action spectra early in the investigation of new areas of photobiological research in an attempt to determine the wavelength limits of the radiation region causing the studied response.

Ultraviolet mutagenesis of radiation-sensitive (rad) mutants of the nematode Caenorhabditis elegans.

A mutational tester strain (JP10) of the nematode C. elegans was used to capture recessive lethal mutations in a balanced 300 essential gene autosomal region. The probability of converting a radiation interaction into a lethal mutation was measured in young gravid adults after exposure to fluences of 254-nm ultraviolet radiation (UV) ranging from 0 to 300 Jm-2.

An SV40 mammalian inductest for putative carcinogens.

This paper describes an in vitro mammalian inductest for putative carcinogens. Several chemical agents were tested using this system which relies on the induction of Simian virus 40 from SV40-transformed hamster kidney cells as an indicator of potential carcinogenic hazard. Aflatoxin B1, sterigmatocystin and aflatoxin G1 were found to be the most efficient inducers in this system followed by the polycyclic hydrocarbons 9,12-dimethylbenzanthracene and benzo[a]pyrene.

Action spectrum for the in vitro induction of simian virus 40 by ultraviolet radiation.

A line of simian virus 40-transformed hamster kidney cells was exposed to ultraviolet radiation at eleven different wavelengths in the region 238-302 nm. An action spectrum derived from the resulting exposure-response curves for the induction of simian virus 40 from these cells exhibits a broad peak in the region 260-270 nm suggesting DNA as the major chromophore for this response. This conclusion is consistent with results obtained by other investigators who have noted viral induction by a number of DNA-damaging agents.

Tumor virus induction and host cell capacity inactivation: possible in vitro tests for photosensitizing chemicals.

The responses of two in vitro mammalian virus-host cell systems to the photosensitizing chemicals proflavine sulfate and 8-methoxypsoralen (8-MOP) in the presence of light are described. Infectious simian virus 40 (SV40) could be induced from SV40-transformed hamster cells by treatment with proflavine plus visible light or 8-MOP plus near UV radiation. The same photosensitizing treatments inactivated the capacity of monkey cells to support the growth of herpes simplex virus.

Mammalian cell viral capacity: an alternative assay for ultraviolet radiation damage.

A comparison is made between the use of colony forming ability and the capacity of cells to produce viruses following infection (called capacity) as assays for the response of mammalian cells to UV radiation. Experiments using two different types of mammalian cells, a rapidly growing, good colony forming monkey kidney cell line (CV-1P) and a slowly growing human skin fibroblast line that was a relatively poor and variable colony former (XP25RO), were conducted using both assay systems. Viral capacity was found to be a more consistent indicator of UV damage to cultured cells than was colony forming ability, especially for the XP25RO cells.

A comparison of herpes simplex virus plaque development after viral treatment with anti-DNA or antilipid agents.

The plaque development of Herpes simplex virus type 1 (HSV) is slower for viruses treated with two anti-DNA agents: ultraviolet radiation (UV) or n-acetoxy-2-acetyl-aminofluorene. For HSV treated with three antimembrane agents--butylated hydroxytoluene, acridine plus near UV radiation, or ether--the plaque development time is the same as for untreated viruses. These differences hold even for viruses that survived treatment that lowered viability below the 1% level.

An effect of cell-culture passage on ultraviolet-enhanced viral reactivation by mammalian cells.

The ability of ultraviolet-irradiated African green monkey kidney cells to reactivate UV-damaged herpes simplex virus was tested over a range of 57 passages (24-81). Several types of controls were employed to minimize daily variations. The results indicate that in this system cells demonstrate an increasing efficiency to reactivate UV-damaged virus until approx.