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ToxSci Advance Access originally published online on November 16, 2005
Toxicological Sciences 2006 89(2):386-398; doi:10.1093/toxsci/kfj045
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Published by Oxford University Press 2005.

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

Miyoung Yoon*,{dagger}, Michael C. Madden{dagger} and Hugh A. Barton{ddagger},1

* National Research Council Research Associateship Program, {dagger} National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Chapel Hill North Carolina 27599–7315; and {ddagger} National Center for Computational Toxicology, Office of Research and Development, U.S. Environmental Protection Agency, Research Triangle Park, North Carolina 27711

Received September 7, 2005; accepted November 9, 2005

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 day 1, 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 postnatal day 1 (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 age dependent.

Key Words: aldehyde dehydrogenase; postnatal development; liver versus lung comparison; propanal; hexanal; benzaldehyde.


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