Abstract
The hypothesis that free radical damage to proteins accelerates overall protein catabolism in and around mammalian cells is discussed. It is concluded that most cells are in possession of sufficient antioxidants to control protein damage, so that changing radical fluxes do not greatly change intracellular protein turnover rates. Exceptions exist however, and may be relevant to specialised cells, and to certain pathologies, where free radical damage to proteins may occur outside cells. The cases of inflammatory disease and atherosclerosis are mentioned, and it is argued that therapies based on anti-oxidant supply may be valuable in these cases.
| Original language | English |
|---|---|
| Pages (from-to) | 361-375 |
| Number of pages | 15 |
| Journal | Revisiones sobre biología celular : RBC |
| Volume | 21 |
| Publication status | Published - 1989 |
| Externally published | Yes |