Molecular cloning of fish alcohol dehydrogenase cDNA

Funkenstein, Bruria; Jakowlew, Sonia B.

doi:10.1016/0378-1119(96)00513-6

Cited by 14 publications

(13 citation statements)

References 12 publications

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“…Expression pattern and activity ADH3 has been described as a ubiquitous enzyme in vertebrates (Ang et al, 1996;Funkenstein and Jakowlew, 1996), although differences in activity in mammalian tissues (up to 30-fold) and, at the transcriptional level, during fish development (up to five-fold) have been reported (Funkenstein and Jakowlew, 1996;Uotila and Koivusalo, 1997). Indeed, from our data, the widespread expression during zebrafish development was not ubiquitous, but consistent with spatio-temporal regulation (Dasmahapatra et al, 2001;Cañ estro et al, 2003).…”

Section: Evolution Of the Mdr-adh Familysupporting

confidence: 66%

Merging protein, gene and genomic data: the evolution of the MDR-ADH family

Gonzàlez‐Duarte

Albalat

2005

Heredity

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Multiple members of the MDR-ADH (MDR: Medium-chain dehydrogenases/reductases; ADH: alcohol dehydrogenase) family are found in vertebrates, although the enzymes that belong to this family have also been isolated from bacteria, yeast, plant and animal sources. Initial understanding of the physiological roles and evolution of the family relied on biochemical studies, protein alignments and protein structure comparisons. Subsequently, studies at the genetic level yielded new information: the expression pattern, exon-intron distribution, in silico-derived protein sequences and murine knockout phenotypes. More recently, genomic and EST databases have revealed new family members and the chromosomal location and position in the cluster of both the first and new forms. The data now available provide a comprehensive scenario, from which a reliable picture of the evolutionary history of this family can be made.

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Section: Evolution Of the Mdr-adh Familysupporting

confidence: 66%

Merging protein, gene and genomic data: the evolution of the MDR-ADH family

Gonzàlez‐Duarte

Albalat

2005

Heredity

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“…Ethanol is metabolized to acetaldehyde by the enzyme alcohol dehydrogenase (ADH) and acetaldehyde is further metabolized to acetate by the enzyme aldehyde dehydrogenase (ALDH). Fish embryos express both ADH and ALDH enzymes during development (Frankel, 1987;Danielsson et al, 1992, Funkenstein andJakowlew, 1996;Dasmahapatra et al, 2001;Reimers et al, 2004b;Wang et al, 2005). During the metabolism of alcohol, superoxide ions are generated inducing embryonic oxidative stress.…”

Section: Discussionmentioning

confidence: 99%

Japanese medaka (Oryzias latipes): developmental model for the study of alcohol teratology

Wang

Williams

Haasch

et al. 2006

Birth Defects Research Pt B

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BACKGROUND: Animal models are necessary to investigate the mechanism of alcohol-induced birth defects. We have used Japanese medaka (Oryzias latipes) as a non-mammalian model to elucidate the molecular mechanism(s) of ethanol teratogenesis. METHODS: Medaka eggs, within 1 hr post-fertilization (hpf) were exposed to waterborne ethanol (0-1000 mM) in hatching solution for 48 hr. Embryo development was observed daily until 10 days post-fertilization (dpf). The concentration of embryonic ethanol was determined enzymatically. Cartilage and bones were stained by Alcian blue and calcein, respectively and skeletal and cardiovascular defects were assessed microscopically. Genetic gender of the embryos was determined by PCR. Levels of two isoenzymes of alcohol dehydrogenase (Adh) mRNAs were determined by semi-quantitative and real-time RT-PCR. RESULTS: The concentration of ethanol required to cause 50% mortality (LC 50 ) in 10 dpf embryos was 568 mM, however, the embryo absorbed only 15-20% of the waterborne ethanol at all ethanol concentrations. The length of the lower jaw and calcification in tail fin cartilaginous structures were reduced by ethanol exposure. Active blood circulation was exhibited at 501 hpf in embryos treated with 0-100 mM ethanol; active circulation was delayed and blood clots developed in embryos treated with 200-400 mM ethanol. The deleterious effects of ethanol were not gender-specific. Moreover, ethanol treatment was unable to alter the constitutive expression of either Adh5 or Adh8 mRNA in the medaka embryo. CONCLUSIONS: Preliminary results suggested that embryogenesis in medaka was significantly affected by ethanol exposure. Phenotypic features normally associated with ethanol exposure were similar to that observed in mammalian models of fetal alcohol syndrome. The results further indicated that medaka embryogenesis might be used as an alternative non-mammalian model for investigating specific alterations in gene expression as a means to understand the molecular mechanism(s) of ethanol-induced birth defects.

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“…The liver ADH of zebrafish is most similar to the ADH3 reported from Sparus aurata (3). Two ADH3 isozymes have been characterized from cod where the h form (high activity toward ethanol) and l form (low activity) differ such that the l form is more similar structurally and functionally to other vertebrate ADH3s (12).…”

Section: Figmentioning

confidence: 95%

“…Alcohol exposure of zebrafish (Danio rerio) embryos during their development produced FAS-like abnormalities of the face, eye, ear, and heart similar to that seen in mammals (2). Only one full-length cDNA sequence from a teleost fish (Sparus aurata) has been reported in the literature (3), and nucleotide sequences in the zebrafish EST database that are identified as ADHs are incomplete and their relationship to other ADH gene products is unclear.…”

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confidence: 97%