Abstract:
:Various antihyperlipemic peroxisome proliferators are known to be carcinogenic in rodents but not in human, other primates and guinea pig, which species lost their ability to synthesize ascorbate due to mutations in the gulonolactone oxidase gene. Ascorbate synthesis is accompanied by H2O2 production, consequently its induction can be potentially harmful; therefore, the in vivo effect of the peroxisome proliferator clofibrate was investigated on gulonolactone oxidase expression in mouse liver. Liver weights and peroxisomal protein contents were increased upon clofibrate treatment. Elevated plasma ascorbate concentrations were found in clofibrate-treated mice due to the higher microsomal gulonolactone oxidase activities. Remarkable gulonolactone oxidase activity appeared in the peroxisomal fraction upon the treatment. Increased activity of the enzyme was associated with an elevation of its mRNA level. According to the present results the evolutionary loss of gulonolactone oxidase may contribute to the explanation of the missing carcinogenic effect of peroxisome proliferators in humans.
journal_name
FEBS Lettjournal_title
FEBS lettersauthors
Braun L,Mile V,Schaff Z,Csala M,Kardon T,Mandl J,Bánhegyi Gdoi
10.1016/s0014-5793(99)01184-9keywords:
subject
Has Abstractpub_date
1999-09-24 00:00:00pages
359-62issue
3eissn
0014-5793issn
1873-3468pii
S0014-5793(99)01184-9journal_volume
458pub_type
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