168
J. KIEFER
Most of the features reviewed so far can be interpreted by ELKIND'S
"repair and progression" model [12]. Briefly, he postulates that the minimum is due to further progression of the irradiated cells along their normal
cycle, whereas the first rise in the curve represents true recovery. The data
quoted are not at variance with this model, but it offers no explanation for
the nature of the process itself.
III. Recovery from Potentially Lethal Damage
In 1953 STAPLETON and his colleagues found that the fraction of E. coli
surviving a given dose of X-rays is a function of post-irradiation incubation
temperature with each strain possessing its own optimum [49]. The authors
offered an explanation which is still very attractive; it will be referred to
below. Even earlier, in 1949, the phenomenon of photoreactivation was
discovered by KELNER [29]: The lethal action of UV irradiation can be
partly reversed if the cells are subjected additionally to visible light.
We shall restrict our considerations to these two phenomena: modification of the survival level by post-irradiation treatments after UV and
X-irradiations, and photoreactivation, keeping in mind that the matter is
far more complex than this, but space and time do not allow a broader
discussion. In this connection we may refer to the excellent reviews given
at the Cortina Congress on host cell reactivation by WINKLER [51], chromosome aberration and repair by EVANS [17], and the genetic aspects of recovery by RORSCH et al. [45].
Our present knowledge on photoreactviation has recently been summarized by JANE SETLOW [47]: under the action of visible light a special photoproduct of UV, thymine-dimers in the cellular DNA, may be split by an
enzyme the nature of which is as unknown as the intrinsic mechanism. The
protein in question has been purified and prepared in an amount which
allowed recording of its absorption spectrum-no appreciable absorption
could be seen at the peak of the action spectrum of photorectivation [39].
There are many postirradiation treatments which alter the survival
level, the best investigated one being the so-called "liquid holding recovery" (LHR), sometimes also named "delayed plating recovery" or "dark
repair", in contrast to photoreactivation, as it does not require light. The
technique is basically very simple: irradiated cells are held in minimal
medium (tap water in the simplest case) for 48-72 hrs before plating. By
this treatment a considerable increase in survival is achieved. The resulting
curves were claimed to result from "normal" ones by a simple dose modification (multiplying the dose by a constant factor) [41], butthis statement
could not be confirmed [4]. LHR has been studied most extensively in
yeast yielding the following very significant results: The process is temperature- and pH-sensitive, showing a pronounced optimum for both. It is
J. KIEFER
Most of the features reviewed so far can be interpreted by ELKIND'S
"repair and progression" model [12]. Briefly, he postulates that the minimum is due to further progression of the irradiated cells along their normal
cycle, whereas the first rise in the curve represents true recovery. The data
quoted are not at variance with this model, but it offers no explanation for
the nature of the process itself.
III. Recovery from Potentially Lethal Damage
In 1953 STAPLETON and his colleagues found that the fraction of E. coli
surviving a given dose of X-rays is a function of post-irradiation incubation
temperature with each strain possessing its own optimum [49]. The authors
offered an explanation which is still very attractive; it will be referred to
below. Even earlier, in 1949, the phenomenon of photoreactivation was
discovered by KELNER [29]: The lethal action of UV irradiation can be
partly reversed if the cells are subjected additionally to visible light.
We shall restrict our considerations to these two phenomena: modification of the survival level by post-irradiation treatments after UV and
X-irradiations, and photoreactivation, keeping in mind that the matter is
far more complex than this, but space and time do not allow a broader
discussion. In this connection we may refer to the excellent reviews given
at the Cortina Congress on host cell reactivation by WINKLER [51], chromosome aberration and repair by EVANS [17], and the genetic aspects of recovery by RORSCH et al. [45].
Our present knowledge on photoreactviation has recently been summarized by JANE SETLOW [47]: under the action of visible light a special photoproduct of UV, thymine-dimers in the cellular DNA, may be split by an
enzyme the nature of which is as unknown as the intrinsic mechanism. The
protein in question has been purified and prepared in an amount which
allowed recording of its absorption spectrum-no appreciable absorption
could be seen at the peak of the action spectrum of photorectivation [39].
There are many postirradiation treatments which alter the survival
level, the best investigated one being the so-called "liquid holding recovery" (LHR), sometimes also named "delayed plating recovery" or "dark
repair", in contrast to photoreactivation, as it does not require light. The
technique is basically very simple: irradiated cells are held in minimal
medium (tap water in the simplest case) for 48-72 hrs before plating. By
this treatment a considerable increase in survival is achieved. The resulting
curves were claimed to result from "normal" ones by a simple dose modification (multiplying the dose by a constant factor) [41], butthis statement
could not be confirmed [4]. LHR has been studied most extensively in
yeast yielding the following very significant results: The process is temperature- and pH-sensitive, showing a pronounced optimum for both. It is