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Liver peroxisomes in newborns from clofibrate-treated rats. II. A biochemical study of the recovery period

The fatty-acyl-CoAβ-oxidation (FAO) and catalase activities, as well as membrane fluidity of liver peroxisomes of newborns from normal and clofibrate-treated rats were studied during the recovery period, ie, throughout the first week of postnatal life. In the test animals the enzyme activities, whic...

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Bibliographic Details
Published in:Biology of the cell 1992, Vol.74 (3), p.315-324
Main Authors: Sartori, Claudia, Stefanini, Stefania, Cimini, Annamaria, Di Giulio, Antonio, Cerù, Maria Paola
Format: Article
Language:English
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Summary:The fatty-acyl-CoAβ-oxidation (FAO) and catalase activities, as well as membrane fluidity of liver peroxisomes of newborns from normal and clofibrate-treated rats were studied during the recovery period, ie, throughout the first week of postnatal life. In the test animals the enzyme activities, which are significantly higher than controls at birth return to normal levels showing a somewhat different time course with FAO rapidly decreasing to control values within three days but with catalase still higher than controls at day 6. The half-life and degradation rate ( K d) of FAO are identical to those calculated by us for the whole organelles and to those reported by others for total catalase in normal or clofibrate-treated adult animals in the presence of catalase inhibitors. Soluble catalase shows turnover values which are similar though not identical to those of FAO, while total catalase has a very long half-life and a low K d. Peroxisomal membrane fluidity, as determined by fluorescence anisotropy of 1-anilinonaphthalene-8-sulfonate (ANS) bound to purified peroxisomal fractions is higher in tests than in controls, recovering normal values within 6 days. Our results demonstrate that liver peroxisomes of rats prenatally exposed to clofibrate return to control conditions within about 1 week. The turnover parameters of enzymes and the membrane fluidity values are discussed in terms of disposal mechanism(s) for the excess of induced peroxisomes.
ISSN:0248-4900
1768-322X
DOI:10.1016/0248-4900(92)90043-Z