Sodium pyrophosphate

Sodium pyrophosphate (12 mg/4 g broth) increases the levels of dialyzable iron and ionic iron in ferric pyrophosphate-fortified broth cubes during in vitro simulated digestion experiments^[1].
Sodium pyrophosphate (2 mM; 12 h) significantly increases the gastric digestibility of myofibrillar protein gels prepared from oxidatively damaged porcine longissimus dorsi muscle, but does not alter their intestinal digestibility^[2].
Sodium pyrophosphate (2 mM; 12 h) increases the β-sheet content in undigested myofibrillar protein gels prepared from oxidatively damaged porcine longissimus dorsi muscle, which helps enhance gastric digestibility, and the protein undergoes a typical structural transition to β-turn during gastrointestinal digestion^[2].
Sodium pyrophosphate (2 mM; 12 h) alters the microstructure of oxidatively damaged myofibrillar protein gels from porcine longissimus dorsi muscle, making it similar to that of non-oxidized gels; it also generates gastric digestion products with a rougher, more porous structure, which is associated with improved digestibility^[2].
Sodium pyrophosphate (2 mM; 12 h) shifts the molecular distribution of gastrointestinal digestion products of oxidatively damaged porcine longissimus dorsi myofibrillar protein gels toward smaller peptide fragments, reduces particle size, and increases the absolute negative value of ζ-potential^[2].
Sodium pyrophosphate (4 mM; 15-90 min) inhibits anti-complementary DNA synthesis and stabilizes DNA-RNA hybrids during poliovirus RNA cDNA synthesis catalyzed by avian myeloblastosis virus reverse transcriptase, thereby increasing the yield of full-length 18S poliovirus cDNA^[3].
Sodium pyrophosphate (4 mM; 10-60 min) inhibits avian myeloblastosis reverse transcriptase-mediated degradation of isolated poliovirus DNA-RNA hybrids and suppresses anti-complementary DNA synthesis using this hybrid as a template^[3].
Sodium pyrophosphate (4 mM; 5-60 min) maintains the nuclease resistance of isolated poliovirus DNA-RNA hybrids during incubation with avian myeloblastosis virus reverse transcriptase, even in the absence of active DNA synthesis^[3].
Sodium pyrophosphate significantly enhances the Fe²⁺ chelating activity and free radical scavenging activities (ABTS, DPPH, hydroxyl free radical) of the digested products from oxidatively damaged porcine longissimus dorsi myofibrillar protein gels after gastric digestion and gastrointestinal digestion^[2].
Sodium pyrophosphate (2 mM; 12 h) increases the contents of total free amino acids, antioxidant amino acids and negatively charged amino acids in gastrointestinal digestion products of myofibrillar protein gels from oxidatively damaged porcine longissimus dorsi, while reduces the contents of essential amino acids and hydrophobic amino acids^[2].
Continuous stimulation with sodium pyrophosphate (50-400 mM; 1 h) induces random mutations in phage SA3821, generating mutant strain SA3821M, which exhibits enhanced bactericidal activity against Staphylococcus aureus CCARM 3821 and improved thermal stability, whereas phage SA3956 remains unaffected under these conditions^[4].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.