Sodium citrate (Natrocitral) is the sodium salt of citric acid.Citric acid trisodium induces apoptosis and cell cycle arrest at G2/M phase and S phase. Sodium citrate cause oxidative damage of the liver by means of the decrease of antioxidative enzyme activities.

Sodium citrate (12.5 mM; 72 h) induces apoptosis and cell cycle arrest at G2/M phase and S phase in a dosedependent manner. Citric acid trisodium (12.5 mM; 48 h) increases the expression of FAS, BAX, BID, AIF, EndoG, cytochrome c, PARP, GADD153, GRP78 and caspase-3, -8, -9, and decreases of BCL-2 and BCL-Xl [1].

Sodium Citrate is the sodium salt of citrate with alkalinizing activity. Upon absorption, sodium citrate dissociates into sodium cations and citrate anions; organic citrate ions are metabolized to bicarbonate ions, resulting in an increase in the plasma bicarbonate concentration, the buffering of excess hydrogen ion, the raising of blood pH, and potentially the reversal of acidosis. In addition, increases in free sodium load due to sodium citrate administration may increase intravascular blood volume, facilitating the excretion of bicarbonate compounds and an anti-urolithic effect [2].