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Clinical Chemistry 43: 273-278, 1997;
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(Clinical Chemistry. 1999;43:273-278.)
© 1999 American Association for Clinical Chemistry, Inc.

Articles

Stability of long-chain and short-chain 3-hydroxyacyl-CoA dehydrogenase activity in postmortem liver

Daniel E. Hale1,a, John E. Cornell2 and Michael J. Bennett3

1 Department of Pediatrics, University of Texas Health Science Center at San Antonio, 7703 Floyd Curl Dr., San Antonio, TX 78284.

2 Geriatric Research, Education and Clinical Center and the South Texas Veterans Health Care System, Audie L. Murphy Division; and Department of Medicine, University of Texas Health Science Center at San Antonio, San Antonio, TX 78284.

3 Departments of Pathology and Pediatrics, University of Texas Southwestern Medical Center, Children's Medical Center of Dallas, 1935 Motor St., Dallas, TX 75235.
a Author for correspondence. Fax 210-567-6921; e-mail hale{at}uthscsa.edu

Inherited enzyme defects in mitochondrial fatty acid oxidation (FAO) are associated with acute metabolic crisis and sudden death. Necropsy findings may be subtle, yielding no diagnosis and precluding genetic counseling. Preliminary identification of an FAO disorder requires the use of sophisticated tools (e.g., GC/MS) and specific body fluids, and the diagnosis rests on molecular analysis or enzyme assay. At present, confirmation of long-chain or short-chain 3-hydroxyacyl-CoA dehydrogenase deficiency relies on measurement of enzyme activity. Here, we report our examination of the effect of storage temperature (25, 4, -20, and -70 °C) and the postmortem interval on enzyme activities in rat and human liver. Enzyme activity decreases 50% in 30 h in samples stored at 25 °C, whereas 55 h at 4 °C is required to reach this value; freezing minimizes this loss. Regardless of rate of degradation, however, the short-chain to long-chain activity ratio remains constant—which should make it possible to differentiate postmortem degradation from enzyme deficiency.


Key Words: indexing terms: sudden infant death syndrome • fatty acid oxidation • inherited metabolic disease • pediatric chemistry • sample handling • rats






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