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. But due to the severe absorption of ultraviolet (UV) radiation by biological samples, UV action spectra were first limited to small cells (bacteria and fungi). Advances in techniques (e.g. single cell culture) and analysis allowed accurate action spectra to be reported even for mammalian cells. But precise analytical action spectra are often difficult to obtain when large, pigmented, or groups of cells are investigated. Here some action spectra are limited in interpretation and merely supply a wavelength vs effect curve. When polychromatic sources are employed, the interpretation of action spectra is even more complex and formidable. But such polychromatic action spectra can be more directly related to ambient responses. Since precise action spectra usually require the completion of a relatively large number of careful experiments using somewhat sophisticated equipment over a range of at least six wavelengths, they are often not pursued. But they remain central to the elucidation of the effect being studied. The worldwide community has agreed that stratospheric ozone is depleting, with the possibility of a consequent rise in the amount of UV-B (290-320 nm) reaching the earth's surface. It is therefore essential that new action spectra be completed for UV-B effects on a large variety of responses of human, animal, and aquatic plant systems. Combining these action spectra with the known amounts of UV-B reaching the biosphere can give rise to solar UV effectiveness spectra that, in turn, can give rise to estimates of effect. Preliminary estimates suggest that ozone layer depletion may seriously impact such important biological end-points as skin cancer, cataracts, the immune system, crop yields, and oceanic phytoplankton. So action spectra continue to play a central role in important photobiological research.

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. In principle, this test is similar to a bacterial inductest and the results obtained in the mammalian inductest are compared to those obtained for the same compounds in the bacterial inductest. In addition, SV40 induction is known to occur in response to ultraviolet radiation and ultraviolet radiation plus the photosensitizing drug, 8-methoxypsoralen.

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. SV40 induction and inactivation of host cell capacity for herpesvirus growth might be useful as screening systems for testing the photosensitizing potential of chemicals. Advantages and disadvantages associated with each system are discussed.

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. Apparent advantages and disadvantages of the use of capacity as an indicator of UV radiation damage are discussed.

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. Gamma ray inactivation of HSV produces no change in plaque development even though this agent is believed to preferentially affect viral DNA.