BRS2 → BRS3 — One-Carbon to Redox Coupling
One-carbon transsulfuration supplies cysteine that BRS3 uses in glutathione-centred redox defence.
Dependency
BRS2 can divert homocysteine through transsulfuration toward cysteine. That cysteine is a substrate for glutathione synthesis. The resulting glutathione pool is used in BRS3 peroxide reduction, electrophile conjugation and related thiol chemistry.
Principal Routes
| Route | Contribution to BRS3 | Relationship |
|---|---|---|
| Transsulfuration (CBS/CTH) | Provides cysteine from homocysteine | Direct |
| Glutathione synthesis from cysteine | Supplies GSH for glutathione-dependent redox enzymes | Direct |
Network Interpretation
This is a substrate-routing dependency, not an immune-regulation pathway. Methyl-cycle flux can compete with transsulfuration, so one-carbon allocation can constrain glutathione precursor supply. The same glutathione pool later conditions BRS1 only as a mediated BRS2 → BRS3 → BRS1 route, not as a BRS2 monoamine-synthesis output.
Boundary and Evidence Status
Transsulfuration and glutathione synthesis are established biochemistry. Substrate availability does not guarantee increased GSH or improved inflammatory outcomes. The dependency does not establish a clinical redox treatment.
Supporting Evidence
- Kumar et al., 2017 — Reviews transsulfuration from homocysteine to cysteine and onward glutathione-related chemistry.
- Chiang et al., 1996 — Reviews SAMe-dependent methylation and the allocation of one-carbon flux that can feed transsulfuration.
- Lu, 2013 — Reviews glutathione synthesis and cysteine as a frequent constraint on that pathway.