Biological oxidations are almost exclusively metal ion-promoted reactions and in ths respect iron, being the most abundant, is the commonly involved. The effect of dietary iron levels on pork, turkey and chick muscle lipid peroxidation and various other related compounds were evaluated. Crossbred feeder pigs were fed to market weight on corn-soy rations containing either 62, 131 or 209 ppm iron. After slaughter, the muscles were dissected, cooked and stored at 4°C. Heavily fortifying swine rations with iron (>200 ppm) increase nn-heme iron (NHI), thiobarbituric acid reactive substances (TBARS), and decrease a-tocopherol in cooked stored pork but did not increase warmed-over aroma (WOA). NHI and TBARS were higher in cooked pork from pigs fed high-iron diets. Liver iron correlated with muscle iron. TBARS were strongly related with WOA. The role of dietary vitamin E and ascorbic acid on Fe-induced in vivo lipid peroxidation in swine was also evaluated. Moderate elevation in iron stores had a marked effect on oxidative stress, especially as indicated by liver TBARS. Supplemental vitamin E, and to a lesser extent vitamin C, protect against this oxidative stress. Unsupplementation of Fe in the regular diet of turkeys did not affect body weight, blood hemoglobin level, or iron pool in the liver or muscle. The reason being that it contained "natural" ~120 mg Fe/kg feed, and this amount is high enough to keep constant the pool of iron in the body, liver or muscle tissues. Only Fe-supplementation with high amounts of Fe (500 ppm) significantly increased turkey blood hemoglobin and total iron in the liver, in 1 out of 3 experiments, but only slightly affects iron pool in the muscles. It seems that the liver accumulates very high concentations of iron and significantly regulates iron concentration in skeletal muscles. For this reason, it was very difficult to decrease muscle stability in turkeys through a diet containing high levels of Fe-supplementation. It was shown that the significant increase in the amount of iron (total and "free") in the muscle by injections with Fe-dextran accelerated its lipid peroxidation rate and decreased its a-tocopherol concentration. The level and metabolism of iron in the muscles affects the intensity of in vivo lipid peroxidation. This process was found to ifluence the turnover and accumulation of a-tocopherol in turkey and chick muscles. Treatments which could significantly decrease the amount and metabolism of iron pool in muscle tissues (or other organs) may affect the rate of lipid peroxidation and the turnover of a-tocopherol. Several defense enzymes were determined and found in the turkey muscle, such as superoxide dismutase, catalase, and glutathione peroxidase. Glutathione peroxidase was more active in muscles with a high trend of lipid peroxidation, lmore so in drumsticks than in breast muscles, or muscles with a low a-tocopherol content. The activity of glutathione peroxidase increased several fold in muscle stored at 4°C. Our work demonstrated that it will be much more practical to increase the stability of muscle tissues in swine, turkeys and chickens during storage and processing by increasing the amount of vitamin E in the diet than by withdrawing iron supplementation.
Effects of dietary vitamin E on microsomal lipid peroxidation and glutathione peroxidase in rat liver.
