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the decrease in the injury to living cells caused by ultraviolet radiation when the cells are subsequently exposed to bright visible light.

Photoreactivation was discovered in 1948 by I. F. Kovalev in the USSR and A. Kelner and R. Dulbecco in the USA as a result of experiments carried out on infusoria paramecia, rotifers, fungous conidia, bacteria, and bacteriophages.

The basis of photoreactivation is the enzymatic splitting (into monomers) of the pyrimidine dimers formed in the deoxyribonucleic acid (DNA) under the action of ultraviolet radiation. Photoreactivation developed in the course of evolution as a protective adaptation against the lethal effects of the ultraviolet component of solar radiation. It is one of the most important forms of repair of injuries to the genetic system in living organisms.


Kovalev, 1. F. “Vliianie vidimogo uchastka spektra luchistoi energii na dinamiku patologicheskogo protsessa v kletke, povrezhdennoi ul’trafioletovymi luchami.” In Uchenye zapiski Ukrainskogo eksperimental’nogo instituta glaznykh boleznei, vol. 1. Odessa, 1949.
Vosstanovlenie kletok ot povrezhdenii. Moscow, 1963. (Translated from English.)
Smith, K., and P. Hanawalt. Molekuliarnaia fotobiologiia. Moscow, 1972. (Translated from English.)
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Photoreactivation and dark repair in UV-treated microorganisms: Effect of temperature.
Many experts believe medium pressure, a more costly option, is better because of the possibility of photoreactivation.
The strain contains mutations that render it deficient in photoreactivation (phr-1) and excision repair (uvrA6) (Karentz and Lutze, 1990), and thus, highly sensitive to UV.
Enzymatic photoreactivation is a direct mechanism to repair UV-induced cyclobutane pyrimidine dimers.
Because visible light may cause photoreactivation of UV-damaged microorganisms, we stored collected samples in a dark box, blocked from visible light.
This leaves sensitive targets, such as cell organelles, nuclei, or DNA, exposed to UV-B radiation without enabling immediate repair by photoreactivation.