ReviewMolecular and cellular biochemistry1997
On the molecular etiology of decreased arachidonic (20:4n-6), docosapentaenoic (22:5n-6) and docosahexaenoic (22:6n-3) acids in Zellweger syndrome and other peroxisomal disorders.
Review in Molecular and cellular biochemistry, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
13 citing papers in PubMed, 61 citations in OpenAlex.
- Docosahexaenoic acid and retinal function in children with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency.Journal of inherited metabolic disease · 1999Trial
- A novel FADS2 isoform identified in human milk fat globule suppresses FADS2 mediated Δ6-desaturation of omega-3 fatty acids.Prostaglandins, leukotrienes, and essential fatty acids · 2018Article
- Article
- Lipidomics for studying metabolism.Nature reviews. Endocrinology · 2016Review
- The fatty acid desaturase 2 (FADS2) gene product catalyzes Δ4 desaturation to yield n-3 docosahexaenoic acid and n-6 docosapentaenoic acid in human cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- A role for peroxisome proliferator-activated receptor γ coactivator 1 (PGC-1) in the regulation of cardiac mitochondrial phospholipid biosynthesis.The Journal of biological chemistry · 2014Article
- Review
- Contribution of fetal MR imaging in the prenatal diagnosis of Zellweger syndrome.AJNR. American journal of neuroradiology · 2006Article
- Developmental genetic malformations of the cerebral cortex.Current neurology and neuroscience reports · 2003Review
- Polyunsaturated fatty acid deficiency during dietary treatment of very long-chain acyl-CoA dehydrogenase deficiency. Rescue with soybean oil.Journal of inherited metabolic disease · 2001Article
- Mechanisms of resistance to pathogenesis in muscular dystrophies.Molecular and cellular biochemistry · 1999Review
- Dietary management of long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency (LCHADD). A case report and survey.Journal of inherited metabolic disease · 1999Article
- Polyunsaturated fatty acid synthesis and release by brain-derived cells in vitro.Journal of molecular neuroscience : MNReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alterations in the metabolism of arachidonic (20:4n-6), docosapentaenoic (22:5n-6), and docosahexaenoic (22:6n-3) acids and other polyunsaturated fatty acids in Zellweger syndrome and other peroxisomal disorders are reviewed. Previous proposals that peroxisomes are necessary for the synthesis of 22:6n-3 and 22:5n-6 are critically examined. The data suggest that 22:6n-3 is biosynthesized in mitochondria via a channelled carnitine-dependent pathway involving an n-3-specific delta-4 desaturase, while 20:4n-6, 20:5n-3 and 22:5n-6 are synthesized by both mitochondrial and microsomal systems; these pathways are postulated to be interregulated as compensatory-redundant systems. Present evidence suggests that 22:6n-3-containing phospholipids may be required for the biochemical events involved in successful neuronal migration and developmental morphogenesis, and as structural cofactors for the functional assembly and integration of a variety of membrane enzymes, receptors, and other proteins in peroxisomes and other subcellular organelles. A defect in the mitochondrial desaturation pathway is proposed to be a primary etiologic factor in the clinicopathology of Zellweger syndrome and other related disorders. Several implications of this proposal are examined relating to effects of pharmacological agents which appear to inhibit steps in this pathway, such as some hypolipidemics (fibrates), neuroleptics (phenothiazines and phenytoin) and prenatal alcohol exposure.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.