Conjugated linoleic acid and fish oil in laying hen diets: effects on egg fatty acids, thiobarbituric acid reactive substances, and tocopherols during storage.

The effects of incorporating conjugated linoleic acid (CLA) and fish oil in laying hen diets on egg CLA, n-3 fatty acid, tocopherol, and TBA reactive substances (TBARS) during 60 d of storage were investigated. Hens were fed corn-soybean meal-based diets containing 3% yellow grease (YG), 2.75% yellow grease + 0.25% CLA (YG-CLA), 2.5% yellow grease + 0.25% CLA + 0.25% fish oil (YG-CLA-FO), or 2.75% yellow grease + 0.25% fish oil (YG-FO). Eggs were collected and stored at 4 degrees C up to 60 d. On storage d 0, 20, 40, and 60, eggs (n = 8) from each treatment were selected randomly, and tocopherol and TBARS contents were measured. Egg total lipid and fatty acids were determined on d 0 and 60 of storage. Feeding YG-CLA-FO led to a 5.4 and 7.7% reduction in egg total lipids on d 0 and 60 (P < 0.05) when compared with YG eggs. The YG-CLA and YG-CLA-FO diets led to a 12% increase in egg saturated fatty acids compared with YG eggs. The content of monounsaturated fatty acids were lower ( > 19%) in YG-CLA and YG-CLA-FO compared with YG. Egg n-3 was highest in YG-FO eggs and lowest in YG eggs (P < 0.0001). Storage over 60 d led to a 20 and 67% depletion of CLA in the YG-CLA and YG-CLA-FO eggs (P < 0.0001). A 29% reduction was observed in the total n-3 fatty acid content of YG-CLA-FO eggs at d 60 of storage when compared with d 0 of storage (P < 0.0001). Diet and storage increased TBARS (P < 0.0001), which was highest in YG-CLA eggs at 60 d of storage. The YG-CLA and YG-CLA-FO diets reduced alpha and gamma-tocopherol contents at all days of storage compared with YG eggs (P < 0.05). Regardless of diet, egg storage for 40 d or longer depleted egg tocopherol contents (P < 0.05). These data demonstrate that healthy eggs with increased n-3 fatty acids and CLA can be generated by minor diet modifications, but added tocopherol supplementation may be needed to reduce lipid peroxidation when n-3 or CLA is included in the hen diet.

Burn and smoke inhalation injury in sheep depletes vitamin E: kinetic studies using deuterated tocopherols.

To test the hypothesis that burn and smoke injury will deplete tissue alpha-tocopherol and cause its faster plasma disappearance, deuterium-labeled vitamin E was administered to sheep exposed to both surface skin burn and smoke insufflation, which cause injuries similar to those of human victims of fire accidents. Two different protocols were used: (1) deuterated vitamin E was administered orally with food at time 0 (just before injury) or (2) the labeled vitamin E was administered orally with food the day before injury. The animals, which had been operatively prepared seven days before, were anesthetized and then received both 40% body surface area third-degree burn and 48 breaths of cotton smoke or sham injuries. All were resuscitated with Ringer's lactate solution (4 ml/kg/% BSA burn/24 h) and mechanically ventilated. Blood samples were collected at various times after vitamin E dosing. In both studies the depletion of plasma alpha-tocopherol was faster in the injured sheep. The sheep given deuterated vitamin E 24 h before injury had similar maximum alpha-tocopherol concentrations at similar times. The exponential rates of alpha-tocopherol disappearance were 1.5 times greater and half-lives were 12 h shorter (p < 0.05) in the injured sheep. In separate studies, various tissues were obtained from sheep that were sacrificed from 4 to 48 h after injury. The liver alpha-tocopherol concentrations in sheep killed at various times after injury seem to show a linear decrease at a rate of 0.1 nmol alpha-tocopherol/g liver per hour, suggesting that the liver is supplying alpha-tocopherol to maintain the plasma and lung alpha-tocopherol concentrations, but that this injury is so severe the liver is unable to maintain lung alpha-tocopherol concentrations. These findings suggest that alpha-tocopherol should be administered to burn patients to prevent vitamin E depletion and to protect against oxidative stress from burn injury.