Effects of maternal vitamin E and selenium status during the perinatal period on age-related changes in heart, lung and liver microsomal lipid peroxidation in rat pups.
Female Long-Evans rats of breeding age were acclimated to one of four experimental diets differing in their vitamin E (E) and selenium (Se) contents. These animals were bred and the offspring produced were nursed by their respective dams from birth through 21 days postpartum. Rat pups were killed at postpartum intervals of 4, 9, 14 and 21 days and heart, lung and liver tissue used for isolation of microsomes. Microsomes were used for quantitation of E content as well as for assays of lipid peroxidation (thiobarbituric acid reactive products formation) using an ascorbate/ADP nonenzymatic assay system. Microsomal E content was lower in heart and lung tissues of rat pups at each postpartum interval compared with maternal levels. Liver microsomal E was higher in rat pups at day 4 postpartum compared with maternal levels. Significant differences (P < 0.05) in microsomal E content of rat pup tissues were associated with maternal vitamin E status during the perinatal period and not to differences in dietary Se. In vitro lipid peroxidation was highest in rat pups nursing dams of low E status, the magnitude of which was greatest in heart and liver microsomes. Lung microsomes, in contrast, peroxidized at very low rates compared with heart and liver microsomes. These effects were independent of maternal Se status. Microsomal lipid peroxidation in tissues of rat pups was lowest at the earliest postpartum interval studied (4 days) and, in general, increased with postpartum age. Reduced glutathione did not inhibit lipid peroxidation in heart or lung microsomes but was effective in this respect in liver microsomes of rat pups as early as 4 days postpartum.
Pazak
H E
HE
Department of Veterinary Science, Pennsylvania State University, University Park 16802, USA.
Scholz
R W
RW
D000375:Aging / Q000378:metabolism*; D000824:Animal Nutritional Physiological Phenomena; D000818:Animals; D000831:Animals, Newborn / Q000378:metabolism*; D005260:Female; D015227:Lipid Peroxidation / Q000502:physiology*; D008099:Liver / Q000378:metabolism; D008168:Lung / Q000378:metabolism; D008431:Maternal-Fetal Exchange; D008861:Microsomes / Q000737:chemistry / Q000378:metabolism*; D009206:Myocardium / Q000378:metabolism; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000378:metabolism*; D011297:Prenatal Exposure Delayed Effects; D051381:Rats; D012643:Selenium / Q000008:administration & dosage / Q000493:pharmacokinetics*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D014810:Vitamin E / Q000008:administration & dosage / Q000493:pharmacokinetics*
D017392:Thiobarbituric Acid Reactive Substances; D014810:Vitamin E; D012643:Selenium