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ToxSci Advance Access originally published online on November 8, 2006
Toxicological Sciences 2007 95(1):89-97; doi:10.1093/toxsci/kfl142
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© The Author 2006. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Expression Profiling of Heat Stress Effects on Mice Fed Ergot Alkaloids

Sachin Bhusari*, Zhilin Liu*, Leonard B. Hearne{dagger}, Donald E. Spiers*, William R. Lamberson* and Eric Antoniou*,1

* Division of Animal Sciences, University of Missouri-Columbia, Columbia, MO 65211 {dagger} Department of Statistics, University of Missouri-Columbia, Columbia, Missouri 65211

1 To whom correspondence should be addressed at S140A, Animal Science Research Center, Columbia, Missouri, 920 East Campus Drive. Fax: 573-882-6827. E-mail: antonioue{at}missouri.edu.

Received August 31, 2006; accepted October 20, 2006


  Abstract

Fescue toxicosis affects wild and domestic animals consuming ergot alkaloids contained in tall fescue forage infected with the endophytic fungus, Neotyphodium coenophialum. When animals are consuming infected fescue (E+) forage during periods of elevated ambient temperatures (summer), a range of phenotypic disorders collectively called summer slump is observed. It is characterized by hyperthermia, with an accompanying decrease in feed intake, growth, milk yield, and reproductive fitness. Laboratory mice also exhibit symptoms of fescue toxicosis at thermoneutral (TN) temperature, as indicated by reduced growth rate and reproductive fitness. Our goal was to characterize the differences in gene expression in liver of mice exposed to summer-type heat stress (HS) and E+ when compared to mice fed E+ at TN temperature. Mice were fed E+ diet under HS (34 ± 1°C; n = 13; E+HS) or TN conditions (24 ± 1°C; n = 14; E+TN) for a period of 2 weeks between 47 and 60 days of age. Genes differentially expressed between E+HS versus E+TN were identified using DNA microarrays. Forty-one genes were differentially expressed between treatment groups. Expressions of eight genes were measured using quantitative real-time PCR. Genes coding for phase I detoxification enzymes were upregulated in E+HS mouse liver. This detoxification pathway is known to produce reactive oxidative species. We observed an upregulation of genes involved in the protection against reactive oxidative species. Key genes involved in de novo lipogenesis and lipid transport were also upregulated. Finally, genes involved in DNA damage control and unfolded protein responses were downregulated.

Key Words: microarray; environmental toxicology; gene expression/regulation.


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[Abstract] [Full Text] [PDF]


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