Valorizing fish processing waste: Production of protein hydrolysates from milkfish (Chanos chanos) by-products using acid hydrolysis

Milkfish (Chanos chanos) by-products were used as raw material for the production of protein hydrolysates. Acid hydrolysis was performed at 121 °C for 90 min at 15 psi using various concentrations of hydrochloric acid (4, 6, and 8M). The protein hydrolysates were characterized for the degree of hydrolysis (DH), and antioxidant and other functional food properties. The yield obtained ranged from 5.14±0.42% to 6.08±1.53%. High DH was observed at a high acid concentration with 43.88±9.50% DH for 8M HCl. Regarding the functional food properties, solubility of over 80% over a wide range of pH (2-12) was observed, and emulsifying and foaming properties were found to depend on the pH (2-10). As for the antioxidant activity, 8M exhibited the highest antioxidant activity among the three treatments. The results showed that milkfish by-products have potential to serve as raw material for protein hydrolysates that can be used as ingredients for food formulations

Morphine induces preconditioning via activation of mitochondrial KCa channels

PURPOSE: Mitochondrial calcium sensitive potassium (mK(Ca)) channels are involved in cardioprotection induced by ischemic preconditioning. In the present study we investigated whether morphine-induced preconditioning also involves activation of mK(Ca) channels. METHODS: Isolated rat hearts (six groups; each n = 8) underwent global ischemia for 30 min followed by a 60-min reperfusion. Control animals were not further treated. Morphine preconditioning (MPC) was initiated by two five-minute cycles of morphine 1 muM infusion with one five-minute washout and one final ten-minute washout period before ischemia. The mK(Ca) blocker, paxilline 1 muM, was administered, with and without morphine administration (MPC + Pax and Pax). As a positive control, we added an ischemic preconditioning group (IPC) alone and combined with paxilline (IPC + Pax). At the end of reperfusion, infarct sizes were determined by triphenyltetrazoliumchloride staining. RESULTS: Infarct size was (mean +/- SD) 45 +/- 9% of the area at risk in the Control group. The infarct size was less in the morphine or ischemic preconditioning groups (MPC: 23 +/- 8%, IPC: 20 +/- 5%; each P < 0.05 vs Control). Infarct size reduction was abolished by paxilline (MPC + Pax: 37 +/- 7%, P < 0.05 vs MPC and IPC + Pax: 36 +/- 6%, P < 0.05 vs IPC), whereas paxilline alone had no effect (Pax: 46 +/- 7%, not significantly different from Control). CONCLUSION: Cardioprotection by morphine-induced preconditioning is mediated by activation of mK(Ca) channel