Vitamin B12a monohydrochloride

Vitamin B12a monohydrochloride acts as a cofactor in cells and within the body, participating in key biological processes such as methylation and fatty acid metabolism. It plays a crucial role in nervous system function and erythropoiesis, and can be used in research on treatments related to vitamin B12 deficiency (including pernicious anemia).

Methods: Primary rat hepatocytes were isolated by collagenase perfusion. A 0.5 mM NaSH solution was added to induce toxicity. Concurrently or at a later time, 25–150 μM Vitamin B12a monohydrochloride or 25–100 μM cobalt chloride was added. The samples were incubated at 37°C for 30–180 min, and cell viability was assessed using the trypan blue exclusion assay.
Results: Both vitamin B12a monohydrochloride and cobalt chloride dose-dependently inhibited NaSH-induced hepatotoxicity; 100 μM vitamin B12a monohydrochloride provided the greatest protective effect, with protection still observed when administered 60 min later, though administration within 20 min yielded the best results. [1]
Methods: 0.5 mM NaSH was added to 0.1 M Tris-HCl buffer (pH 7.4), followed by the addition of either 0.1 mM Vitamin B12a monohydrochloride or 0.1 mM cobalt chloride. The oxygen consumption rate was measured using a Clark oxygen electrode, H₂O₂ production was determined by the catalase assay, and hydroxyl radicals were detected by the deoxyribose degradation assay.
Results: Vitamin B12a monohydrochloride significantly promoted NaSH-mediated oxygen consumption and H₂O₂ production (which could be reversed by catalase), did not generate hydroxyl radicals, and exhibited significantly higher catalytic activity than cobalt chloride. [1]

Methods: Male CD1 mice weighing 25–30 g were selected and administered intraperitoneal injections of NaSH (an H₂S donor) at concentrations of 0.45, 0.54, 0.63 mmol/kg, corresponding to LD₅₀, LD₆₅, and LD₈₅, respectively). Two minutes later, Vitamin B12a monohydrochloride (0.25 mmol/kg) was administered intraperitoneally. A saline control group and a nitrite (0.25 mmol/kg) positive control group were established, and mouse survival rates were observed for 24 hours.
Results: Vitamin B12a monohydrochloride significantly improved the survival rate of mice with NaSH poisoning: 100% in the 0.45 mmol/kg NaSH group, 80% in the 0.54 mmol/kg group, and 65% in the 0.63 mmol/kg group; administration of nitrite had no significant protective effect.