Matrical inclusions of peroxisomes induced by clofibrate in preneoplastic hepatocytes of rats fed 3'-methyl-4-dimethyl-aminoazobenzene.
M Gotoh, Yohichi Mochizuki, N Sawada, Hideyuki Tsukada
Abstract
M Gotoh, Yohichi Mochizuki, N Sawada, Hideyuki Tsukada
Abstract
The response of peroxisomes to clofibrate in preneoplastic hepatocytes of rats fed 3'-methyl-4-dimethylaminoazobenzene was examined histochemically (using the 3,3'-diaminobenzidine reaction) and electron microscopically. Morphometrical examinations revealed that the number of peroxisomes correlated well with the intensity of the histochemical reaction. Preneoplastic hepatocytes which responded to clofibrate with a marked proliferation of peroxisomes showed no matrical inclusions or merely matrical plates in very low incidence in the proliferated peroxisomes. The cells that exhibited a moderate proliferation of peroxisomes showed formation of peroxisomal matrical inclusions in high incidence. The inclusions were matrical plates and tubules showing the same fine structures as those found in 2-acetylaminofluorene carcinogenesis. These peroxisomal inclusions were absent in the cells which responded to clofibrate with no or only a slight increase in the number of peroxisomes. It is suggested that these varieties of peroxisomal changes might reflect the progress of preneoplastic phases of the cells.
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The response of peroxisomes to clofibrate in preneoplastic hepatocytes of rats fed 3'-methyl-4-dimethylaminoazobenzene was examined histochemically (using the 3,3'-diaminobenzidine reaction) and electron microscopically. Morphometrical examinations revealed that the number of peroxisomes correlated well with the intensity of the histochemical reaction. Preneoplastic hepatocytes which responded to clofibrate with a marked proliferation of peroxisomes showed no matrical inclusions or merely matrical plates in very low incidence in the proliferated peroxisomes. The cells that exhibited a moderate proliferation of peroxisomes showed formation of peroxisomal matrical inclusions in high incidence. The inclusions were matrical plates and tubules showing the same fine structures as those found in 2-acetylaminofluorene carcinogenesis. These peroxisomal inclusions were absent in the cells which responded to clofibrate with no or only a slight increase in the number of peroxisomes. It is suggested that these varieties of peroxisomal changes might reflect the progress of preneoplastic phases of the cells.
Key concepts: Clofibrate, Peroxisome, Biology, Carcinogenesis, Microbody, Chemistry, Endocrinology, Biochemistry