Abstract
The ultraviolet (UV) absorption spectra of major epidermal chromophores (tryptophan, tyrosine, DNA, and urocanic acid) provide a glimpse of the primary targets of UVB effects. In the case of urocanic acid, the action spectrum is almost superposable with the action spectrum of immuno suppression. The combined action spectra of UVB–UVA irradiation for lethality, mutagenesis, and pyrimidine dimer formation show an abrupt break at about 330 nm. This chapter discusses DNA repair processes. The post replication repair process, which results in DNA daughter strand gaps, requires a complete growth medium with nutrients, whereas nucleotide excision repair occurs in buffer devoid of nutrients. Avoidance of post replication repair by cells in the stationary phase, with nutrients in the growth medium exhausted, results in the higher survival. The damaged part of a DNA molecule can be restored in situ, without breaking its sugar phosphate backbone, by photo reactivation (PR). The enzymatic splitting of cyclobutane-type pyrimidine dimers is mediated by intense blue light. The PR enzyme is DNA photolyase. In the dark, the enzyme binds tightly to a cyclobutane-type dimer to form an enzyme substrate complex. The absorption of light between 300 and 450 nm activates this complex. The pyrimidine dimer is converted to monomeric pyrimidines, and the enzyme is released.
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