Vitamin E deficiency as hepatic peroxisomal proliferator: Electron microscopic evidence

Dabholkar, Arun S.

doi:10.1016/0309-1651(81)90199-5

Cited by 6 publications

(1 citation statement)

References 12 publications

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“…In some tissues, such as the liver, the number and size of peroxisomes vary greatly under the influence of certain drugs, diet, vitamins, or diseases. Striking increases occur, for example, in vitamin E deficiency [17] and during clofibrate treatment [36], while depressed numbers of peroxisomes characterize certain malignancies [75] and cell lines with high rates of anaerobic metabolism [53]. Their overall abundance as well as specific enzyme content appear to be, at least in part, substrate-regulated [75,76].…”

Section: Absent Peroxisomes and Defective Mitochondrial Oxidationmentioning

confidence: 99%

The cerebrohepatorenal syndrome of Zellweger, morphologic and metabolic aspects

Kelley

1983

Am. J. Med. Genet.

169

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The cerebrohepatorenal syndrome of Zellweger (CHRS) is remarkable not only for a distinctive combination of congenital anomalies, but also for an unusual variety of profound metabolic disturbances. After a discussion of the clinical diagnosis of CHRS, abnormalities in the metabolism of peroxisomes, mitochondria, iron, pipecolic acid, glycogen, bile acids, and organic acids are discussed and related to the clinical and other biochemical findings in the syndrome. Attention is also drawn to syndromes with biochemical or clinical abnormalities similar to those of CHRS. Although the biochemical findings indicate major abnormalities in oxidative metabolism, the primary defect remains obscure.

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Section: Absent Peroxisomes and Defective Mitochondrial Oxidationmentioning

confidence: 99%

The cerebrohepatorenal syndrome of Zellweger, morphologic and metabolic aspects

Kelley

1983

Am. J. Med. Genet.

169

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Ultrastructure of Experimental Cocaine Hepatotoxicity

et al. 1986

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Cocaine is a potent hepatotoxin in mice. It is converted in the liver by a minor oxidative pathway to the active metabolite, norcocaine nitroxide. Previous studies have shown evidence of a lipid peroxidative mechanism of toxicity, including increased conjugated diene absorption by hepatic microsomal lipids following a single 60 mg per kg i.p. dose of cocaine in DBA/2Ha mice. To explore this mechanism further, morphologic changes in the livers of DBA/2Ha mice were examined following the same dose of cocaine. The first ultrastructural change seen was dilatation of rough endoplasmic reticulum in centrilobular hepatocytes 1 hr following cocaine injection, coincident with the previously observed onset of increased conjugated diene absorption in microsomal lipids. During the previously observed period of peak conjugated diene absorption (2 to 4 hr), ultrastructural changes in centrilobular hepatocytes progressed. These included focal mitochondrial membrane disruption followed by more extensive mitochondrial swelling and disruption with increased swelling of rough endoplasmic reticulum. Changes in size, shape and concentration of histochemically labeled, morphometrically studied peroxisomes were also seen during this interval. Injury of centrilobular hepatocytes advanced to cell death in 6 to 8 hr. The time course and nature of these morphologic findings correlate with previously observed evidence of lipid peroxidation, supporting the hypothesis that this is the mechanism of cocaine hepatoxicity.

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Ultrastructural localization of catalase and D-amino acid oxidase in ‘normal’ fetal mouse liver

Dabholkar

1986

Experientia

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Vitamin E deficiency as hepatic peroxisomal proliferator: Electron microscopic evidence

Cited by 6 publications

References 12 publications

The cerebrohepatorenal syndrome of Zellweger, morphologic and metabolic aspects

The cerebrohepatorenal syndrome of Zellweger, morphologic and metabolic aspects

Ultrastructure of Experimental Cocaine Hepatotoxicity

Ultrastructural localization of catalase and D-amino acid oxidase in ‘normal’ fetal mouse liver

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