Lipid oxidation in high-pressure processed chicken breast muscle during chill storage: critical working pressure in relation to oxidation mechanism

The oxidative stability of chicken breast muscle subjected to high-pressure treatment at 300, 400, 500, 600, 700 or 800 MPa for 5 min or 10 min, or to heat treatment (80 degrees C for 10 min) and subsequent storage at 5 degrees C was evaluated over a 2-week period. Lipid oxidation in pressure-treated chicken breast muscle monitored as formation of thiobarbituric acid reactive substances depended to a high degree on the working pressure and less on the pressurizing time. The pressure treatment at 800 MPa for 10 min was found to enhance lipid oxidation to the same extent as the heat treatment. Pressure treatment at 600 MPa and 700 MPa resulted in less oxidation. Chicken breast muscle exposed to pressure at or below 500 MPa showed no indication of rancidity, similar to what was found for untreated meat during chill storage; accordingly 500 MPa is a critical pressure for pressure treatment of chicken breast muscle. Analysis of non-heme iron in pressure-treated chicken breast muscle revealed that the notable increase in lipid oxidation caused by high pressure above 500 MPa did not result from the release of iron ions during high-pressure treatment. Furthermore, no influence of high-pressure treatment on the catalytic activity of metmyoglobin on lipid oxidation was observed in a model system? and it is concluded that increased lipid oxidation is probably related to membrane damage.