Table 2.
Description of (putative) intracellular oxidative stress effects observed after CAP and their representation by corresponding detected proteins.
| Oxidative stress-related effects | Consequences | Immediate effects | Long-term responses | Examples from our study |
|---|---|---|---|---|
| Protein damages | Unfolding | Loss of function | Elimination and subsequent new production | Proteasome-related proteins↑ (PRS4, PSME1, PSME2) |
| Misfolding | Heat shock protein interaction | Refolding and/or repair | Translational activity ↑ (CH60, ENPL, GRP78, HS90A, HS71A, HSPB1) | |
| Decomplexation/dimerization | pI shifts | Heat shock proteins↓ (HS105, HSP74, AHSA1) | ||
| Shifts in molecular weight | PDIA 1, 3, 4, 6↑ | |||
|
| ||||
| DNA damages | Single-strand scissions | Detection mechanisms | SOS repair | MRE11↑ |
| Double-strand scissions | Damage marking | Apoptosis | PPP6↓ | |
| Base modifications | Cell cycle arrest | Cancer development | MSH2↓ | |
| Hydrolysed bonds between sugar and base | KU86↓, RD23A↓, RD23B↑, RUVB1↓, RUVB2↓ | |||
|
| ||||
| Detoxification of reactive oxygen species (ROS) | H2O2 detoxification | Catalase active | Regeneration of “exhausted” proteins | (Catalase not found) |
| OH● detoxification | Peroxidases active | Appearance of isoforms | PRDX2↓, 3↓, 4↑ | |
| O2-● detoxification | Superoxide dismutase active | SODC↓ | ||
| Thioredoxin system active | TRXR1↑, TXND5, TXNL5↑ | |||
| Glutathione system active | GSTO1↓, GSTP1↓, GLRX3↓ | |||
|
| ||||
| Membrane modifications | Membrane oxidation | Structural changes | Changes in permeability | |
| Lipid peroxidation | Increased/decreased protein integration | Changes of the membrane potential | AL1B1↓ | |
| Transporter proteins | Apoptosis | CLIC4↓ | ||
Possible damages of proteins, nucleic acids, and lipids may result in cellular responses, which are exemplarily listed as logical consequences. Corresponding identified proteins and their regulation modes (up- or downregulated) are indicated.