Isolation and characterization of a Chinese hamster ovary cell line deficient in fatty alcohol:NAD+ oxidoreductase activity

Paul F. James, William B Rizzo, Jongsoon Lee, Raphael A. Zoeller

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

We have isolated a mutant Chinese hamster ovary cell line that is defective in long-chain fatty alcohol oxidation. The ability of the mutant cells to convert labeled hexadecanol to the corresponding fatty acid in vivo was reduced to 5% of the parent strain. Whole-cell homogenates from the mutant strain, FAA.1, were deficient in long-chain fatty alcohol:NAD+ oxidoreductase (FAO; EC 1.1.1.192) activity, which catalyzes the oxidation of hexadecanol to hexadecanoic acid, although the intermediate fatty aldehyde was formed normally. A direct measurement of fatty aldehyde dehydrogenase showed that the FAA.1 strahl was defective in this component of FAO activity. FAA.1 is a two-stage mutant that was selected from a previously described parent strain, ZR-82, which is defective in ether lipid biosynthesis and peroxisome assembly. Because of combined defects in ether lipid biosynthesis and fatty alcohol oxidation, the ability of the FAA.1 cells to incorporate hexadecanol into complex lipids was greatly impaired, resulting in a 60-fold increase in cellular fatty alcohol levels. As the FAO deficiency in FAA.1 cells appears to be identical to the defect associated with the human genetic disorder Sjögren-Larsson syndrome, the FAA.1 cell line may be useful in studying this disease.

Original languageEnglish (US)
Pages (from-to)6102-6106
Number of pages5
JournalProceedings of the National Academy of Sciences of the United States of America
Volume87
Issue number16
DOIs
StatePublished - Jan 1 1990

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long-chain-alcohol dehydrogenase
Fatty Alcohols
Cricetulus
Ovary
Cell Line
long-chain-aldehyde dehydrogenase
Lipids
Ether
Inborn Genetic Diseases
Peroxisomes
Palmitic Acid
Medical Genetics
Fatty Acids

Keywords

  • Fatty alcohol metabolism
  • Sjögren-Larsson syndrome
  • Somatic cell mutant

ASJC Scopus subject areas

  • General

Cite this

Isolation and characterization of a Chinese hamster ovary cell line deficient in fatty alcohol:NAD+ oxidoreductase activity. / James, Paul F.; Rizzo, William B; Lee, Jongsoon; Zoeller, Raphael A.

In: Proceedings of the National Academy of Sciences of the United States of America, Vol. 87, No. 16, 01.01.1990, p. 6102-6106.

Research output: Contribution to journalArticle

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AB - We have isolated a mutant Chinese hamster ovary cell line that is defective in long-chain fatty alcohol oxidation. The ability of the mutant cells to convert labeled hexadecanol to the corresponding fatty acid in vivo was reduced to 5% of the parent strain. Whole-cell homogenates from the mutant strain, FAA.1, were deficient in long-chain fatty alcohol:NAD+ oxidoreductase (FAO; EC 1.1.1.192) activity, which catalyzes the oxidation of hexadecanol to hexadecanoic acid, although the intermediate fatty aldehyde was formed normally. A direct measurement of fatty aldehyde dehydrogenase showed that the FAA.1 strahl was defective in this component of FAO activity. FAA.1 is a two-stage mutant that was selected from a previously described parent strain, ZR-82, which is defective in ether lipid biosynthesis and peroxisome assembly. Because of combined defects in ether lipid biosynthesis and fatty alcohol oxidation, the ability of the FAA.1 cells to incorporate hexadecanol into complex lipids was greatly impaired, resulting in a 60-fold increase in cellular fatty alcohol levels. As the FAO deficiency in FAA.1 cells appears to be identical to the defect associated with the human genetic disorder Sjögren-Larsson syndrome, the FAA.1 cell line may be useful in studying this disease.

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