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An intracellular organelle found in all eukaryotes except the archezoa (original lifeforms). In electron micrographs, peroxisomes appear round with a diameter of 0.1–1.0 micrometer, although there is evidence that in some mammalian tissues peroxisomes form an extensive reticulum (network). They contain more than 50 characterized enzymes and perform many biochemical functions, including detoxification. See Cell organization, Enzyme

Peroxisomes are important for lipid metabolism. In humans, the β-oxidation of fatty acids greater than 18 carbons in length occurs in peroxisomes. In yeast, all fatty acid β-oxidation occurs in peroxisomes. Peroxisomes contain the first two enzymes required for the synthesis of plasmalogens. Peroxisomes also play important roles in cholesterol and bile acid synthesis, purine and polyamine catabolism, and prostaglandin metabolism. In plants, peroxisomes are required for photorespiration. See Lipid metabolism, Photorespiration

A number of recessively inherited peroxisomal disorders have been described and grouped into three categories. Group I is the most severe and is characterized by a general loss of peroxisomal function. Many of the enzymes normally localized to the peroxisome are instead found in the cytosol. Among the diseases found in group I are Zellweger syndrome, neonatal adrenoleukodystrophy, and infantile Refsum disease. Patients with these disorders usually die within the first years after birth and exhibit neurological and hepatic (liver) dysfunction, along with craniofacial dysmorphism (malformation of the cranium and the face). Groups II and III peroxisomal disorders are characterized by a loss of peroxisomal function less severe than in group I.


(cell and molecular biology)
Any of a subclass of microbodies that contain at least four enzymes involved in the metabolism of hydrogen peroxide.
References in periodicals archive ?
The researchers moved peroxisomes around in the cell using a sophisticated laboratory technique, with the same result.
Genetic heterogeneity consisting of 14 CGs has been identified in PBDs by cell-fusion CG analysis using fibroblast cell lines derived from PBD patients (5), (20), (25)-(27) (Table 3), where the primary cause for PBDs was revealed to be the impaired biogenesis of peroxisomes.
The expression levels of 10 genes: retinoid X receptor alpha (RXRA), peroxisome proliferator-activated receptor gamma (PPARG), phospholipid transfer protein (PLTP), stearoylCoA desaturase (SCD), nuclear receptor subfamily 1 group H member 3 (NR1H3), fatty acid binding protein 3 (FABP3), carnitine palmitoyltransferase II (CPT2), acyl-Coenzyme A dehydrogenase long chain (ACADL), acyl-Coenzyme A oxidase 2 branched chain (ACOX2), and fatty acid binding protein 4 (FABP4), showed significant differences in gene expression between the low- and high-marbled groups (p < 0.
BACKGROUND: Trichloroacetic acid, an oxidative metabolite of trichloroethylene (TRI), is a ligand of the peroxisome proliferator-activated receptor [alpha] (PPAR) [alpha], which is involved in lipid homeostasis and anti-inflammation.
Direct demonstration that the deficient oxidation of very long chain fatty acids in X-linked adrenoleukodystrophy is due to an impaired ability of peroxisomes to activate very long chain fatty acids.
Peroxisomes, which are intracellular organelles and contain more than 50 enzymes involved in diverse biochemical processes, were chosen as a test-bed for the idea because they are relatively poorly characterized, play a central role in human metabolism and are linked to a number of human health concerns including aging, cancer, heart disease, obesity, diabetes, and neurological disorders.
Phthalates can activate the three peroxisome proliferator--activated receptor (PPAR) isotypes on cellular models and induce peroxisome proliferation in rodents.
According to this hy pothesis, the proliferation of peroxisomes leads to the generation of free radicals, which can result in damage to the cell's DNA and, eventually, cancer.
Relationship between morphological changes and lipid lowering action of p-chlorphenoxyisobutyric acid (CPIB) on hepatic mitochondria and peroxisomes in man.
Instead, they trigger the liver to produce peroxisomes -- 15 to 20 times the normal number.
Initially, it was hypothesized that the proliferation of peroxisomes themselves was causally related to cancer (e.
They are glycogen poor from the start with increased numbers of mitochondria, peroxisomes, and ribosomes.

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