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ToxSci Advance Access published online on November 16, 2005
Toxicological Sciences, doi:10.1093/toxsci/kfj045
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Published by Oxford University Press 2005.
Received September 7, 2005
Accepted November 9, 2005

Biotransformation and Toxicokinetics

Developmental Expression of Aldehyde Dehydrogenase in Rat: A Comparison of Liver and Lung Development

Miyoung Yoon 1, Michael C. Madden 2, and Hugh A. Barton 3 *

1 National Research Council Research Associateship Program at US Environmental Protection Agency, Human Studies Facility, 104 Mason Farm Rd., Md#58B, Chapel Hill NC 27599-7315; National Health and Environmental Effects Research Laboratory, Human Studies Facility, 104 Mason Farm Rd., Md#58B, Chapel Hill NC 27599-7315
2 National Health and Environmental Effects Research Laboratory, Human Studies Facility, 104 Mason Farm Rd., Md#58B, Chapel Hill NC 27599-7315
3 National Center for Computational Toxicology, Office of Research and Development, US Environmental Protection Agency, 109 TW Alexander Dr. Research Triangle Park, MD B143-01, NC 27711, USA

* To whom correspondence should be addressed.
Hugh A. Barton, E-mail: habarton{at}alum.mit.edu


  Abstract

Metabolism is one of the major determinants for age-related changes in susceptibility to chemicals. Aldehydes are highly reactive molecules present in the environment that also can be produced during biotransformation of xenobiotics and endogenous metabolism. Although the lung is a major target for aldehyde toxicity, early development of aldehyde dehydrogenases (ALDHs) in lung has been poorly studied. The expression of ALDH in liver and lung across ages (postnatal day1, 8, 22, and 60) was investigated in Wistar-Han rats. In adult, the majority of hepatic ALDH activity was found in mitochondria while cytosolic ALDH activity was the highest contributor in lung.

Total aldehyde oxidation capability in liver increases with age, but stays constant in lung. These overall developmental profiles of ALDH expression in a tissue appear to be determined by the different composition of ALDH isoforms within the tissue and their independent temporal and tissue-specific development. ALDH2 showed the most notable tissue-specific development. Hepatic ALDH2 was increased with age, while the pulmonary form did not. ALDH1 was at its maximum value at PND1 and decreased thereafter both in liver and lung. ALDH3 increased with age in liver and lung, although ALDH3A1 was only detectible in lung. Collectively, the present study indicates that in the case of aldehyde exposure, the in vivo responses would be tissue and agedependent.

Keywords: Aldehyde dehydrogenase; postnatal development; Liver vs. Lung comparison; propanal; hexanal; benzaldehyde.

Disclaimer: The research described in this article has been reviewed by the National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency and approved for publication. Approval does not signify that the contents necessarily reflect the views and policies of the Agency nor does mention of trade names or commercial products constitute endorsement or recommendation for use.


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