Microbodies in Experimentally Altered Cells
نویسندگان
چکیده
A rapid and sustained increase in the number of microbodies in liver and kidney cells can be induced in male rats by ethyl chlorophenoxyisobutyrate (CPIB), a hypolipidemic drug. This phenomenon permits investigation of several aspects of microbody behavior in experimental conditions. Reversal experiments demonstrate that liver cells revert to normal between 2 and 3 weeks after withdrawal of CPIB and that one of the mechanisms for removal of excess microbodies is their incorporation into structures indistinguishable from lysosomes. In a state of rapid cell division, such as that present during liver regeneration, microbody proliferation apparently occupies a high biological priority. In necrotic or degenerating cells microbody structure remains relatively normal. The increase in microbodies induced by CPIB is inhibited by chloramphenicol. No increase in microbodies occurred in female rats or in chickens, guinea pigs, or rabbits at the dosage used (0.25% in diet). No changes in microbodies were seen in monkey liver. Catalase activity was generally parallel to the numerical response in microbodies. Additional observations suggest that the microbody response to CPIB is not related to hepatomegaly induced by this agent but may be related to the hypolipidemic effect of CPIB, though hypolipidemia per se is not a specific or sufficient cause of microbody proliferation.
منابع مشابه
MICROBODIES IN EXPERIMENTALLY ALTERED CELLS VII. CPIB-induced Hepatic Microbody Proliferation in the Absence of Significant Catalase Synthesis
Previous studies (1-3) demonstrated a significant increase in number of microbodies (peroxisomes) and concomitant elevation in catalase activity in male rat liver following administration of ethyl-o, p-chlorophenoxyisobutyrate (clofibrate, CPIB), a hypolipidemic drug that lowers serum cholesterol and triglycerides in man (4) and in experimental animals (5, 6) . Neither the significance of micro...
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ورودعنوان ژورنال:
- The Journal of Cell Biology
دوره 40 شماره
صفحات -
تاریخ انتشار 1967