QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text (PDF) Purchase Article View Shopping Cart Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Maeda, Y. Articles by Matsuzawa, Y. Search for Related Content PubMed PubMed Citation Articles by Maeda, Y. Articles by Matsuzawa, Y.

Biotin Deficiency Decreases Ornithine Transcarbamylase Activity and mRNA in Rat Liver¹

Second Department of Internal Medicine, Osaka University Medical School, 2-2 Yamadaoka, Suita, Osaka 565, Japan

Biotin deficiency is well known as a cause of hyperammonemia, but there has been no report on the effect of biotin deficiency on hepatic ureagenesis. In this study, we examined the changes in the activities and gene expression of urea cycle enzymes using rats fed raw egg white as a model of biotin deficiency. All rats were made biotin-deficient by feeding them an avidin-containing diet for 6 wk. The rats were divided into two groups at the beginning of this experiment: biotin-deficient rats (BD rats) and biotin-supplemented rats (BS rats) which were treated with biotin once a day at a dose of 1 mg per rat intraperitoneally. The plasma ammonia concentration of the BD rats (92.8 ± 12 µmol/L) was significantly higher than that of BS rats (63.9 ± 16 µmol/L, P < 0.05). The activities of ornithine transcarbamylase (OTC) was significantly lower in the liver of the BD (110.2 ± 5.5) rats than in the BS rats (154 ± 3.8 U/mg protein, P < 0.01). Activities of the other urea cycle enzymes were not significantly different in the two groups. OTC gene expression in the liver of BD rats was 40% lower than in BS rats (P < 0.05). These data suggest that biotin deficiency decreases OTC activity and the amount of OTC mRNA.

KEY WORDS: • biotin • urea cycle enzymes • ornithine transcarbamylase • rats • plasma ammonia

¹ The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

² To whom correspondence should be addressed.

Manuscript received 25 April 1995. Revision accepted 31 August 1995.

This article has been cited by other articles:

				A. Perez-Monjaras, R. Cervantes-Roldan, I. Meneses-Morales, R. A. Gravel, S. Reyes-Carmona, S. Solorzano-Vargas, A. Gonzalez-Noriega, and A. Leon-Del-Rio Impaired Biotinidase Activity Disrupts Holocarboxylase Synthetase Expression in Late Onset Multiple Carboxylase Deficiency J. Biol. Chem., December 5, 2008; 283(49): 34150 - 34158. [Abstract] [Full Text] [PDF]

				D. Pacheco-Alvarez, R. S. Solorzano-Vargas, R. A. Gravel, R. Cervantes-Roldan, A. Velazquez, and A. Leon-Del-Rio Paradoxical Regulation of Biotin Utilization in Brain and Liver and Implications for Inherited Multiple Carboxylase Deficiency J. Biol. Chem., December 10, 2004; 279(50): 52312 - 52318. [Abstract] [Full Text] [PDF]

				R. Rodriguez-Melendez, G. Camporeale, J. B. Griffin, and J. Zempleni Interleukin-2 receptor-gamma -dependent endocytosis depends on biotin in Jurkat cells Am J Physiol Cell Physiol, February 1, 2003; 284(2): C415 - C421. [Abstract] [Full Text] [PDF]