SummaryThis study was conducted to investigate whether a moderate running exercise would enhance or prevent the lipid peroxidation in animal body and also stimulate or depress the degradation-excretion of lipid peroxides (LIPOX, thiobarbituric acid reactive substances deter mined as malon dialdehyde) in young female rats. Compared with sedentary rats, voluntary wheel-running exercised rats did not show any significant difference in total LIPOX contents in plasma and several tissues including brain, and whole body during 4 weeks of experiment with a vitamin E-free low LIPOX diet. On the contrary, when rats were previously fed a high LIPOX diet and then allowed voluntary exercise with a vitamin E-added low LIPOX diet, total LIPOX contents per whole body reduced significantly faster in the exercised rats than in the sedentary controls during 2 weeks of exercise. At that period, LIPOX were progressively increased in the brain in both groups of animals, but was significantly greater in the exercised group. Interestingly, more than 80% of total LIPOX contents in whole body were found to be stored in carcass portions regardless of greater or lesser amounts of LIPOX contents in rats. These data suggest that a moderate exercise of several weeks might enhance the degradation-excretion of LIPOX but not the formation accumulation of LIPOX in rats. Exercise also seems to modulate LIPOX transference among tissues.
whether or not the feeding of air-oxidized oil to rat dams during the period of gestation or lactation affects the lipid peroxide contents in their offspring was studied. Rat dams were given a diet containing 4 g soybean oil or air-oxidized soybean oil/ 100 g diet during gestation. Whole body lipid peroxides, thiobarbituric acid-reactive substances (TBARS) determined as malondialdehyde, in newborn pups from dams fed the air-oxidized oil diet were not different from those from dams fed the unoxidized oil diet. When dams were given the oxidized oil diet during lactation, whole body TBARS contents in suckling pups increased sharply in the 10-day-old neonate and decreased until 21 days old. However, these trends were not affected by the amounts of air-oxidized soybean oil nor the unoxidized oil diet. These findings indicate that a maternal diet containing air-oxidized oil during gestation or lactation does not affect the whole body lipid peroxides in neonatal rats.
SummaryTo evaluate lipid peroxide metabolism in neonatal rats during suckling, we studied developmental changes in whole body lipid peroxidation by measurement of thiobarbituric acid-reactive substances (TBARS) determined as malondialdehyde. Whole body TBARS contents were very low immediately after birth but increased sharply at 3-9 days, peaked at 9-15 days, and then remained unchanged until 21 days. The feeding of a skimmed milk diet to neonates between 17 and 20 days old sharply decreased their whole body TBARS contents at 20 days as compared with those at lb days, however, this was not observed by the feeding of an artificial milk diet containing 3 g of soybean oil/ 100 g diet. In vitro ethane production by liver and brain homogenates and in vivo breath ethane levels in expired air were higher at 20 or 21 days than at 10 days after birth. These results suggest that lipid peroxide formation in neonatal rats increases shortly after birth and that its degradation and/or excretion may increase during the latter period of suckling.
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