Ultraviolet (UV) radiation, particularly in the UV-C range (wavelengths around 200-280 nm, with peak germicidal effectiveness around 260-265 nm), is a common physical method for controlling microbial growth (disinfection). The primary mechanism by which UV radiation exerts its antimicrobial effect is by damaging the microorganism's DNA.
- DNA Absorption: Nucleic acids (DNA and RNA) strongly absorb UV radiation at these wavelengths.
- Pyrimidine Dimer Formation: The absorbed energy causes the formation of abnormal covalent bonds between adjacent pyrimidine bases (primarily thymine, but also cytosine) on the same DNA strand. The most common are thymine dimers.
- Disruption of DNA Function: These dimers create kinks or distortions in the DNA helix. This structural damage interferes with essential cellular processes:
- DNA Replication: The distorted DNA cannot be accurately replicated by DNA polymerase, leading to stalled replication forks or errors.
- Transcription: RNA polymerase may also be blocked or misread the damaged template, affecting protein synthesis.
- Mutations and Cell Death: If the DNA damage is extensive or not repaired effectively by the cell's DNA repair mechanisms, it can lead to mutations and ultimately cell death or inactivation.
While very high doses of UV might cause some protein damage (option a, c), its primary and most significant target at germicidal doses is DNA, leading to the disruption of DNA replication and transcription. Cellular dehydration (option d) is typically associated with desiccation, not directly with UV action. \[ \boxed{\text{Disruption of DNA replication}} \]