Lipid oxidation is an increasing problem in stored turkey muscle and other muscle foods. Off-odours and off-flavours (e.g. oxidative rancidity) are the primary forms of quality deterioration that takes place when lipid oxidation is not suppressed during refrigerated and frozen storage of meats. Increased use of corn oil in animal diets from the corn ethanol industry has increased the degree of fatty acid unsaturation in muscle and depot fat. Lipid oxidation increases in general as the fatty acid unsaturation increases. Barrier films in packaging have become thinner which increases the incidence of oxidative rancidity due to greater exposure of oxygen to the packaged meat.
Demand from consumers for meat products without synthetic antioxidants, curing agents, and phosphates has also increased occurrence of lipid oxidation. Another concern is that some synthetic antioxidants in animal feed may soon be banned due to toxicity concerns. Providing less protected feed to animals will lower the storage stability of the resulting meat from the animal.
There are preformed lipid hydroperoxides (LOOHs) in muscle tissue even in vivo. These LOOHs are likely the reactant that leads to off-flavour during storage of meat and fish. Low molecular weight metals (e.g. Fe-ADP and Cu-citrate), haemoglobin, and myoglobin have the ability to decompose LOOH to volatile compounds (e.g. aldehydes, ketones) that collectively impart rancid odours and flavours. Identifying the primary oxidant in turkey muscle can be useful in developing targeted strategies to decrease lipid oxidation during storage.
Dietary vitamin E effectively inhibits lipid oxidation when a threshold concentration is reached in poultry muscle, and it is clear that vitamin E deposits into turkey muscle much less effectively compared to chicken muscle (Marusich et al., 1975).
The mechanism to explain why vitamin E deposits poorly into turkey muscle remains poorly understood.
Research to better understand the mechanism of poor vitamin E accumulation in turkey muscle may lead to strategies to better incorporate vitamin E into muscle, thereby decreasing lipid oxidation during storage.
Effect of natural antioxidants on lipid oxidation in turkey deli loaves
Naturally brewed soy sauce (SS) and Natural Flavour Enhancer (NFE), a product derived from soy sauce with less soy sauce flavour and colour were evaluated in sliced, uncured, turkey deli loaves (Park et al., 2013). SS and NFE inhibited hexanal formation compared to the control after 1 and 7 days of refrigerated storage under vacuum packaged conditions (P<0.05). After day 7 of vacuum packaging, the sliced product was transferred to oxygen permeable bags for an additional 4 days of storage (represented as day 11). This simulates storage by a consumer after opening the package at home. SS and NFE suppressed hexanal formation at day 11 compared to control (P<0.05). Taste and overall acceptability scores were higher in SS and NFE at day 11 compared to control (P<0.05). These studies indicate that SS and NFE can stabilize lipids in uncured and sliced turkey deli meat during refrigerated storage.
Effects of two different natural antioxidants (AO) were investigated in a commercially made deli turkey product either with or without phosphate and compared to a control without AO (Bak and Richards, 2014). The antioxidants examined were Guardian™ 09 and Stabilenhance® OSR D 2.5. The product was uncured and packaged in an atmosphere of N2/CO2 gas. Lipid oxidation was measured after 1, 7, and 13 weeks of refrigerated, dark storage via sensory detection of off-flavour (OF) and headspace hexanal determination by solid-phase micro extraction (SPME) gas chromatography (GC). Without phosphates in the formulation, Guardian and StabEnhance did not effectively inhibit lipid oxidation. With added phosphate, Guardian 09 was the most effective treatment (hexanal values less than 0.5 ppm during 13 weeks of storage). Phosphates can inactivate metals through chelation. If left unchelated by phosphate, those metals can readily oxidize not only lipids but also heme proteins, rendering the heme proteins more oxidative towards lipids. Correlations between hexanal and OF were statistically significant at each time point (P < 0.05). The correlation improved as time of storage increased.
Residual haemoglobin as a pro-oxidant in turkey muscle
Myoglobin is often considered the only heme protein of significance in post mortem muscle. However, residual haemoglobin from blood in breast muscle from chickens was 3.5-7.1 mg/g in the bled group compared to 4.1-9.4 in the unbled group (Griffiths et al., 1985). This indicated some haemoglobin was removed from muscle by bleeding but not much. In bled turkeys, 38% of the total heme protein content in the thigh muscle was haemoglobin (Niewiarowicz et al., 1986). In bled chickens, 64-85% of the total heme protein content in the thigh muscle was haemoglobin (Fleming et al., 1991; Kranen et al., 1999). We have utilized a protein that selectively inactivates the ability of haemoglobin to cause lipid oxidation in finely macerated muscle tissue. Greater than 96% of lipid oxidation that occurred in minced, turkey, thigh muscle was inhibited by the added haemoglobin inhibitor (Grunwald and Richards, 2014). This strongly suggests haemoglobin was the primary oxidant in the macerated, turkey muscle and antioxidant strategies should be directed toward inactivating haemoglobin as an oxidant.
Dietary vitamin E as an antioxidant in turkey muscle
Lipid oxidation occurs rapidly during storage of turkey muscle compared to that of chicken (Gong et al., 2010). We examined the ability of a natural form of dietary vitamin E (RRR-alpha tocopheryl aceate) to deposit in turkey muscle compared to synthetic vitamin E (all-racemic alpha tocopheryl acetate). Natural vitamin E deposited in turkey muscle around 2-fold more effectively compared to synthetic vitamin E (Perez et al., 2012). The mechanism of poor deposition of vitamin E into the muscle of turkeys compared to chickens was examined by measuring tocopherol metabolites in bile from both types of birds. The tocopherol metabolites examined were the product of cytochrome P450 hydroxlyase(s) that hydroxylate the tail portion of vitamin E. After hydroxylation, a series of β-oxidation reactions convert the hydroxylated vitamin E molecule to smaller metabolites. Tocopherol metabolites were up to 8.3-fold higher in turkey compared to chicken bile (Perez et al., 2013). Deposition of vitamin E in turkey muscle was also lower compared to chicken muscle and lipid oxidation occurred more rapidly in the turkey muscle. These findings suggest that elevated CYP450 hydroxylase activity in turkeys leads to decreased accumulation of dietary vitamin E into muscle. It was also found the erythrocytes (e.g. red blood cells) from turkeys were more susceptible to detergent-induced lysis compared to chicken erythrocytes (Perez et al., 2014). Lysis causes the release of haemoglobin from the erythrocyte compartment so that the heme protein is free to oxidize phospholipids that are part of the muscle cell structure.