Sodium sulfite

Sodium sulfite is an inorganic salt used as an antioxidant and preservative. Sodium sulfite is also used in sulfonation and sulfomethylation reactions. Sodium sulfite can also be used as a bleaching agent, desulfurizer, and dechlorinator. Sodium sulfite inhibits hepatocyte proliferation, promotes hepatocyte apoptosis and necrosis, and impairs mitochondrial integrity. Sodium sulfite induces superoxide anion production, primes neutrophils for enhanced superoxide anion generation, and induces neutrophil gene expression. Sodium sulfite can be used in studies related to pulmonary inflammation and gastric tissue injury^[1][2][3]. In Vitro:Sodium sulfite (10^-5-10^-2 M; 24-72 h) alters the morphology of human hepatocytes L02 in a time- and concentration-dependent manner, with notable toxic effects occurring at 10^-3 M and 10^-2 M^[1].
Sodium sulfite (10^-5-10^-2 M; 72 h) inhibits the viability of human hepatocytes L02 in a concentration-dependent manner, with an IC₅₀ of 4.68×10^-4 M after 72 h incubation^[1].
Sodium sulfite (10^-5-10^-2 M; 24-72 h) inhibits the proliferation of human hepatocytes L02 in a time- and concentration-dependent manner, with significant inhibition occurring at concentrations of 5×10^-4 M and higher^[1].
Sodium sulfite (10^-5-10^-2 M; 72 h) induces apoptosis in human hepatocytes L02 in a concentration-dependent manner, with notable apoptosis starting at 10^-4 M and severe cell death occurring at 10^-2 M within 24 h^[1].
Sodium sulfite (4.68×10^-4 M; 72 h) alters the expression of 97 genes in human hepatocytes L02, with 13 genes significantly upregulated and 14 genes significantly downregulated, driving pathways that inhibit cell proliferation, induce apoptosis, and cause mitochondrial damage via reactive oxygen species production^[1].
Sodium sulfite (0.1-10 mM; 5-30 min) concentration-dependently induces superoxide production in freshly isolated human neutrophils within 5 to 30 min, and (0.1-10 mM; 30 min pre-incubation followed by 5 min fMLP stimulation) concentration-dependently primes these neutrophils to enhance fMLP-induced superoxide production following 30 min pre-incubation^[2].
Sodium sulfite (0.1-10 mM; 4 h) concentration-dependently induces RNA synthesis in freshly isolated human neutrophils following 4 h incubation, but does not induce neutrophil shape changes^[2].
Sodium sulfite (0.1-10 mM; 20 h) does not modulate apoptosis rates in freshly isolated human neutrophils following 20 h incubation, nor does it reverse the apoptosis-delaying effect of GM-CSF in these cells^[2].
Sodium sulfite (0.001-10 mM; 5-24 h) induces dose-dependent necrotic cell death in RGM1 cells via oxidative stress, with an IC₅₀ of 0.17 mM, and this cytotoxicity is attenuated by the free radical scavenger Trolox^[3].
Sodium sulfite (0-5 mM; 20 h) induces necrotic cell death in RGM1 cells independent of the apoptotic signaling pathway, as shown by unchanged caspase/PARP cleavage, caspase activity, and DNA fragmentation, alongside dose-dependent LDH release^[3].
Sodium sulfite (0-10 mM; 0-120 min, 24 h) induces oxidative modification, aggregation, and inactivation of purified lysozyme via metal ion-catalyzed free radical formation, independent of superoxide or hydrogen peroxide scavenging^[3].