Sodium sulfite

Sodium sulfite is a biochemical reagent utilized as a biomaterial or organic compound in life science research. Sodium sulfite is commonly employed in biochemical, analytical, and biomaterial-related investigations, where Sodium sulfite serves as a useful reagent for experimental and methodological applications.

Method: Human hepatocyte L02 cells were exposed to sodium sulfite at concentrations ranging from 10⁻⁵ to 10⁻² M for 72 h, and cell viability was evaluated.
Rresult: Sodium sulfite inhibited L02 cell viability in a concentration-dependent manner, with an IC50 of 4.68 × 10⁻⁴ M after 72 h.[1]
Method: Isolated human neutrophils were treated with sodium sulfite, and superoxide production, fMLP-induced oxidative responses, total RNA synthesis, cell morphology, and apoptosis were evaluated.
Rresult: Sodium sulfite directly induced superoxide production within 5 min and concentration-dependently enhanced fMLP-induced superoxide production. It also concentration-dependently increased gene expression within approximately 4 h, but did not induce cell-shape changes or alter neutrophil apoptosis after 20 h.[2]
Method: Rat gastric mucosal RGM1 cells were exposed to sodium sulfite at concentrations of 0–5 mM for 20 h, and cytotoxicity and oxidative-stress markers were evaluated.
Rresult: Sodium sulfite caused significant cytotoxicity in RGM1 cells and increased protein carbonyls, 8-hydroxy-2′-deoxyguanosine, and the accumulation of carbonylated protein aggregates, indicating oxidative protein and DNA damage.[3]
Method: RBL-2H3 mast cells were exposed to 2–8 mM sodium sulfite, and reactive oxygen species generation, pyroptosis-related proteins, membrane integrity, and mast-cell degranulation were evaluated. NAC or MCC950 was used to investigate the involvement of ROS and NLRP3.
Rresult: Sodium sulfite increased ROS generation and the expression of NLRP3, caspase-1, GSDMD-N, IL-1β, and IL-18; induced cell-membrane rupture; and increased β-hexosaminidase and histamine release. NAC and MCC950 attenuated these effects, indicating that sodium sulfite induced mast-cell pyroptosis and degranulation through the ROS/NLRP3 pathway.[4]

Method: Sodium sulfite solutions were used to remove dissolved oxygen and establish a chemically induced hypoxia model in Caenorhabditis elegans.
Rresult: Sodium sulfite generated controllable hypoxic conditions and induced hypoxia-related death, morphological cellular defects, and stabilization of hypoxia-inducible factor 1 in C. elegans, producing responses similar to physical hypoxia.[5]

H2O: 160.00 mg/mL (1269.44 mM), Sonication is recommended.