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Acrylamide Stimulates Glutamine Uptake in Fischer 344 Rat Astrocytes by a Mechanism Involving Upregulation of the Amino Acid Transport System N
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aDepartment of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, North Carolina, USA bDepartment of Neurotoxicology, Medical Research Center, Polish Academy of Sciences, Warsaw, Poland cDepartment of Pediatrics and Pharmacology, and the Kennedy Center, Vanderbilt University Medical Center, Nashville, Tennessee, USA
Address for correspondence: Michael Aschner, Ph.D., Department of Pediatrics, B-3307 Medical Center North, Vanderbilt University School of Medicine, Nashville, TN 37232-2495. Voice: 615-322-8024; fax: 615-322-6541. michael.aschner{at}vanderbilt.edu
High demand of neoplastic tissues for glutamine (Gln) is met by its active transport across cell membranes. Chronic treatment with acrylamide in rodents is associated with an increased incidence of neoplasms, including astrocytomas. In this study, 24-h acrylamide treatment significantly increased the initial rate of l-[G-3H]glutamine uptake in astrocyte cultures derived from the acrylamide-sensitive Fischer 344 rat, and this effect could be fully inhibited by histidine, a model substrate for the amino acid transport system N. RT-PCR analysis revealed that acrylamide treatment caused a significant increase in the astrocytic expression of the mRNA coding for the major system N protein, SNAT3, which is specifically overexpressed in malignant gliomas in situ. The acrylamide-induced upregulation of astrocytic Gln transport via system N is likely to affect Gln homeostasis in these cells and may be causally related to the increased astrocytoma incidence observed in Fischer 344 rats.
Key Words: acrylamide • amino acid transport system N • astrocyte • Fischer 344 rat • glutamine (Gln) This article has been cited by other articles:
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