From the above results, it can be calculated that the two-protein biocatalyst are between four and six times more stable towards oxidative inactivation than the soluble enzyme.
Interestingly, amino acid substitutions were discovered in these two modification sites in pig (T264Q and S478T), such substitutions may make this protein more stable for oxidative biotransformation of various endo- and xenobiotics, and further biomedical studies focusing on the CYP3A4 gene (using the pig as a model) should be aware of such modifications.
Although counterintuitive, covalent modification of an inactive antibiotic by BlmB or TlmB immediately after its biosynthesis may provide a preemptive and complementary mechanism of resistance from self-imposed oxidative damage and/or a more stable, yet potentially reversible, inactivation.
The +5 oxidation state is more stable.
Lipid peroxides and protein oxidation are the secondary products of oxidative stress causing secondary injury by further generating relatively more stable and diffusible cytotoxic agents such as malondialdehyde and 4-hydroxy-trans-2-nonenal, respectively, and magnifying oxidative stress [ 30].
On the other hand, B homologues may either be involved in regulating a cellular function more conserved across organisms, or its involvement in cellular metabolism is not as broad as in a situation of oxidative stress, and therefore these homologues are more stable across organisms throughout geological time.
Protein carbonyls are more advantageous as oxidative stress markers as oxidised proteins are generally more stable.
Free radical scavenging by the low molecular weight compounds can play an important role as the last line of defense against oxidative damage of the cells for they are more stable than enzymatic antioxidant apparatus and can be easily accumulated in stress conditions (e.g deposited in the cell wall or the vacuole).
Oxidation products of proteins such as guanine, guanosine, and deoxyguanosine turn out to be more stable and their determination seems to be more specific in the course of oxidative stress.
