Part F: A Closer Look at....
Biological Consequences of Ultraviolet Exposure
Why is UV bad for your health?
Some UV is necessary for good health. We can only make vitamin D when solar UV
stimulates our skin. Otherwise, we have to add it to our diet. However, most UV, especially the
more energetic photons of UV-B, causes harm. These photons damage our cells and organs by
producing chemical changes in important molecules, especially proteins and nucleic acids. The
lens of the eye is particularly vulnerable. UV absorbed in the lens proteins contributes to the
formation of cataract, which decreases the ability of the lens to transmit light, resulting in partial
or complete blindness. Exposed skin is subject to short-term effects such as sunburn and longer-term effects such as skin cancer and premature aging. The more we are exposed to UV, the more
The long-term effects of UV on living things are caused by changes in the genetic
material, DNA. Large doses of UV may kill a cell outright by creating too much damage in its
DNA. Smaller doses may have lasting effects by causing mutations (changes in the DNA
sequence) or recombination between DNA molecules. Genetic changes such as mutation or
recombination can affect the growth of cells, in some cases, leading to uncontrolled growth or
Interaction between UV and DNA
Although UV photons of different energies have various effects on DNA, the most
important damage to DNA is the formation of pyrimidine dimers. In the pyrimidine dimer, two
adjacent pyrimidine bases--cytosine (C) and/or thymine (T)--are linked in an abnormal structure
(Figure 1A & B) which distorts the shape of the DNA double helix (Figure 2) and blocks its
copying by the DNA replication or RNA transcription machinery. A block in either of these
important processes would be very dangerous for a cell; as little as one dimer per cell in fact, can
be lethal. Dimers are formed in DNA most efficiently by UV-C, less efficiently by UV-B, and
very little by UV-A action.
How cells suffer from and repair pyrimidine dimers is our primary concern, but UV
damages DNA in other ways. Another alteration of the pyrimidine bases, called the 6-4 lesion
because of how the molecule is damaged (Figure 1C), may cause mutations. Other types of base
damage may also occur, but they are not as biologically important as the dimer or 6-4 lesion.
Repair of DNA damage
Cells of all types have evolved mechanisms for repairing DNA damage. These repair
systems deal with damage caused by UV, ionizing radiation, chemical agents in the environment,
and just plain everyday wear-and-tear or spontaneous damage. Scientists have found a surprising
similarity in the DNA repair systems of fairly unrelated organisms. This similarity, or
evolutionary conservation, as a scientist would describe it, tells us two things:
1) repair systems
are so important to organisms of all sorts that they changed little through evolution AND must
have arisen early in the history of life on Earth;
2) we can use "model" organisms to do
experiments that would be difficult to do in larger organisms like people. We use the model
organism bakers' yeast here; yeast is a eukaryote like plants, animals, and humans, but grows as a
single cell like bacteria and so is easy to cultivate. Working with yeast enables you to take
advantage of many years of research other scientists have done on DNA repair processes in this
simple organism. Research suggests that DNA repair processes in humans are very similar to
DNA repair in yeast.
Another clue to the importance of DNA repair is that most living creatures have
developed four different repair processes.
1) Photoreactivation (PR) uses visible light as an
energy source to "un-dimerize" pyrimidine dimers.
2) Excision repair makes use of several
enzymes to remove dimers and resynthesize DNA.
3) Error-prone repair is yet another
enzymatic process that removes dimers, but also makes mistakes, which become mutations in the
4) Recombinational repair occurs when recombination between DNA
molecules rescues cells that have developed gaps when DNA that contains dimers is replicated.
The fate of an irradiated cell
What happens to a cell which has been exposed to UV depends on a number of things. If
the yeast cell is growing on a grape leaf in the sunshine, it can use photoreactivation to rapidly
and accurately repair dimers. The excision repair system is also quite efficient and may find the
dimer and fix it first. If DNA replication is occurring and the dimer is in a region of DNA due to
be replicated, a mutation might occur if the polymerase tries to copy the dimer instead of
stopping; alternatively, if it stops and starts again later leaving a gap, recombination will be
required to repair the gap. You can think of the outcome as being dependent on a race between
the replication machinery and the different repair proteins. Most of the time, the repair proteins
(photoreactivation or excision) win, since even in UV-irradiated cells, mutation and
recombination frequencies are low.
A cell will die if a dimer is not repaired. A cell will live and be unchanged if an error-free system repairs the dimer. A cell will live and may be changed if an error-prone or
recombinational system repairs the damage. If the change (mutation or recombination) alters an
important gene, the cell may die even though the dimer was repaired. In some experiments you
can make use of mutant yeast strains that have lost the ability to carry out several of the repair
processes. As you would expect, these strains are more sensitive to the UV radiation in sunlight,
which makes it easier to do experiments with them.
To Learn More...
Read Repair of DNA
Connections Between Ozone and DNA Damage
To see how it all fits together, consider two more kinds of spectra. One is called the
absorption spectrum for ozone and the other is the action spectrum for damage to DNA.
Recall that a spectrum is a graph of any property plotted against wavelength (or photon energy).
An absorption spectrum for something like ozone, then, would be a graph of how well it absorbs
photons plotted against the wavelength (See Figure 3). Notice that where the ozone absorption is
greatest, the difference between the solar UV and the surface UV is also greatest. 300 DU of
ozone effectively absorbs all the UV-C, more than half of the UV-B, but very little of the UV-A.
Now look at the curve in Figure 3 labeled "DNA Action." This curve is the action
spectrum for DNA damage. Clearly the wavelengths that are most effective at damaging DNA
are also strongly absorbed by ozone. That is extremely fortunate for us. However, notice the
small range of wavelengths around 300 nm where the DNA action spectrum and the surface UV
spectrum overlap. That is the region (labeled "net DNA effect") where the "action" is. Shorter
wavelengths of UV would be more damaging to DNA, but they are removed by the ozone.
Longer wavelengths get through the ozone, but they do not have much effect on DNA.
More UV-B of shorter wavelengths penetrates to the surface as the ozone decreases.
Since these wavelengths are more damaging to DNA than longer ones, the rate of increase of
DNA damage increases as the ozone decreases. In Figure 4 the probability that DNA will be
damaged is plotted against the ozone concentration. At very low ozone values, the probability of
damage would go up catastrophically. The inset shows that in the range of values around 300
DU, the risk of DNA damage increases by 2.5 percent for each 1 percent decrease in the ozone
To Learn More...
Read Modeling the Effects of Ultraviolet Radiation, see Video tape section: Global
Ozone, and explore the UVRISK computer program.
Figure 3: Sunlight, ozone, DNA interactions.
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