Peroxisomal Proliferation in Heart and Liver of Mice Receiving Chlorpromazine, Ethyl 2(5(4-Chlorophenyl)Pentyl) Oxiran-2-Carboxylic Acid or High Fat Diet: A Biochemical and Morphometrical Comparative Study

Vamecq, Jòseph; Roels, Frank; Branden, Christiane Van Den; Draye, Jean‐Pierre

doi:10.1203/00006450-198712000-00027

Cited by 24 publications

(9 citation statements)

References 15 publications

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“…This method has proved to be a suitable and accurate means for analysis of peroxisome proliferation because cytochemical DAB staining can prevent the common underestimation of peroxisomes smaller than 450 nm [10], and because electron microscopic analysis can minimize error caused by overlapping of peroxisomes found in thick sections [10]. The volume density of peroxisomes in the control wild-type mice was estimated to be 1.4%, which is in good agreement with previously reported values of 1.4% [21] and 1.2% [22]. Thus, the results of morphometric analysis are considered to be reasonable.…”

Section: Discussionsupporting

confidence: 87%

Peroxisome proliferator-activated receptor α-independent peroxisome proliferation

Zhang

Tanaka

Nakajima

et al. 2006

Biochemical and Biophysical Research Communications

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Section: Discussionsupporting

confidence: 87%

Peroxisome proliferator-activated receptor α-independent peroxisome proliferation

Zhang

Tanaka

Nakajima

et al. 2006

Biochemical and Biophysical Research Communications

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“…thyroid hormone (Hartl and Just, 1987), retinoic acid (Hertz and Bar-Tana, 1992), fatty diets (Christiansen et al, 1981;Dreyer et al, 1993;Forman et al, 1997;Kliewer et al, 1997;Thomassen et al, 1982;Vamecq et al, 1987), the adrenocortical hormone DHEA-S (review by Depreter et al, 2002;Hertz et al, 1991;Leighton et al, 1987;Milewich et al, 1995;Peters et al, 1996) that activate specific receptors (Mangelsdorf and Evans, 1995). Phytanic acid is a peroxisome proliferator in mice ( Van den Branden et al, 1986).…”

Section: Regulation Of Peroxisome Expressionmentioning

confidence: 97%

Human peroxisomal disorders

Depreter

Espeel

Roels

2003

Microscopy Res & Technique

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Peroxisomes are single membrane-bound cell organelles performing numerous metabolic functions. The present article aims to give an overview of our current knowledge about inherited peroxisomal disorders in which these organelles are lacking or one or more of their functions are impaired. They are multiorgan disorders and the nervous system is implicated in most. After a summary of the historical names and categories, each having distinct symptoms and prognosis, microscopic pathology is reviewed in detail. Data from the literature are added to experience in the authors' laboratory with 167 liver biopsy and autopsy samples from peroxisomal patients, and with a smaller number of chorion samples for prenatal diagnosis, adrenal-, kidney-, and brain samples. Various light and electron microscopic methods are used including enzyme- and immunocytochemistry, polarizing microscopy, and morphometry. Together with other laboratory investigations and clinical data, this approach continues to contribute to the diagnosis and further characterization of peroxisomal disorders, and the discovery of novel variants. When liver specimens are examined, three main groups including 9 novel variants (33 patients) are distinguished: (1) absence or (2) presence of peroxisomes, and (3) mosaic distribution of cells with and without peroxisomes (10 patients). Renal microcysts, polarizing trilamellar inclusions, and insoluble lipid in macrophages in liver, adrenal cortex, brain, and in interstitial cells of kidney are also valuable for classification. On a genetic basis, complementation of fibroblasts has classified peroxisome biogenesis disorders into 12 complementation groups. Peroxisome biogenesis genes (PEX), knock-out-mice, and induction of redundant genes are briefly reviewed, including some recent results with 4-phenylbutyrate. Finally, regulation of peroxisome expression during development and in cell cultures, and by physiological factors is discussed.

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“…Phytanic acid oxidation is also impaired and accumulates in the plasma.13,53 The peroxisomal ß-oxidation enzyme, 3-oxoacyl-coenzyme A thiolase, is present in an unprocessed, precursor form and localizes to a peroxisomal "ghost" cell fraction. 40,6155 Unlike the Zellweger and related syndromes, verylong-chain fatty acids, pipecolic acid, and abnormal bile acids do not accumulate in RCDP. Moreover, peroxi¬ somes can be identified by DAB cytochemistry in tis¬ sues of RCDP.13,40 We also observed DAB-positive organelles in RCDP fibroblasts (Figs 5 and 6).…”

Section: Plasma and Erythrocyte Lipidsmentioning

confidence: 99%

Peroxisomal Abnormality in Fibroblasts From Involved Skin of CHILD Syndrome

Emami¹

1992

Arch Dermatol

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The CHILD, C-H, and rhizomelic chondrodysplasia punctata syndromes are all characterized by ichthyosis, chondrodysplasia punctata, and limb defects, as well as peroxisomal deficiency. Thus, these syndromes may be related pathogenically. Because peroxisomes are involved in prostaglandin metabolism, peroxisomal deficiency may directly contribute to the previously reported alterations in prostaglandin metabolism in fibroblasts of involved skin of fibroblasts.

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Peroxisomal Proliferation in Heart and Liver of Mice Receiving Chlorpromazine, Ethyl 2(5(4-Chlorophenyl)Pentyl) Oxiran-2-Carboxylic Acid or High Fat Diet: A Biochemical and Morphometrical Comparative Study

Cited by 24 publications

References 15 publications

Peroxisome proliferator-activated receptor α-independent peroxisome proliferation

Peroxisome proliferator-activated receptor α-independent peroxisome proliferation

Human peroxisomal disorders

Peroxisomal Abnormality in Fibroblasts From Involved Skin of CHILD Syndrome

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