This study was conducted to determine the effects of partial replacement (40.0%) of sodium chloride by potassium chloride, potassium lactate and calcium ascorbate on quality characteristics of cooked pork ham during cold storage. The cooked pork hams with partial replacement of sodium chloride by potassium chloride and potassium lactate had lower lightness (L*) and higher bitterness than others (p <0.05). However, redness (a*), yellowness (b*) and overall acceptability of sensory properties were not different among the treatments (p >0.05). The partial replacement of sodium chloride by all substitutes leads to increase tenderness (p <0.05). There are no problems in microbiological stability and lipid oxidation of cooked pork hams with 40% replacement of sodium chloride by potassium chloride, potassium lactate and calcium ascorbate during cold storage. Therefore, it is possible to use potassium chloride, potassium lactate and calcium ascorbate as partial substitutes of sodium chloride in cooked pork ham.

Sodium-potassium-chloride co-transporter (NKCC) is a membrane bound channel protein that plays a prominent role in a variety of epithelial absorptive, secretory processes and a direct role in cell volume regulation, in which NKCC transports sodium, potassium, and chloride ions across the cell membrane. It has been known that prostaglandin E2 (PGE2) induces an acute cell lysis of specific hemocyte type, oenocytoid, to release prophenoloxidase into the plasma and ouabain (a specific sodium pump inhibitor) inhibits the oenocytoid cell lysis resulting in preventing phenoloxidase activation. However, it is not clear how the intracellular signaling pathway leads to oenocytoid cell lysis in response to PGE2. This study was designed to analyze functional role of NKCC in the cell lysis to release prophenoloxidase. A gene structure of NKCC was derived from cDNA library of Spodoptera exigua hemocyte, NKCC was expressed in all developmental stages and tissues. A real time quantitative RT-PCR showed that bacterial challenge significantly induced its expression. Specific inhibitors of NKCC, bumetanide and chlorothiazide, clearly prevented the cell lysis in a dose dependent manner. When RNA interference using double stranded RNA (dsRNA) specific to NKCC suppressed its expression, the oenocytoid lysis and PO activation was significantly inhibited in response to PGE2. It also reduced nodule formation to bacterial challenge. These results indicate that NKCC is associated with oenocytoid cell lysis probably by increasing cell volume through inward transport of ions in response to PGE2.