|کد مقاله||کد نشریه||سال انتشار||مقاله انگلیسی||ترجمه فارسی||نسخه تمام متن|
|103455||161380||2016||6 صفحه PDF||سفارش دهید||دانلود رایگان|
• We made a rat model of acute CO2 poisoning and analyzed mRNAs expressed in the brain.
• We selected five candidate genes in the frontal cortex and hypothalamus respectively.
• AGPS, HSPB2 may be involved in the dysfunctional cognition by acute CO2 poisoning.
• PPY, CRHR2 may be involved in the regulation of respiration by acute CO2 poisoning.
• Assays for these mRNAs may help identify acute CO2 poisoning as a cause of death.
Acute carbon dioxide (CO2) poisoning causes no specific features that are revealed upon autopsy, and the pathophysiological mechanism of this syndrome is unclear. To address this issue, in the present study, we exposed rats to CO2 concentrations ranging from 10% to 60% and determined the effects on mRNA expression. According to the results of Gene Ontology (GO) and cluster analyses of microarrays data, we selected the following genes for further analysis: alkylglycerone phosphate synthase (Agps), hypocretin (Hcrt), tyrosine hydroxylase (Th), heat shock protein beta 2 (Hspb2), and opioid receptor delta 1 (Oprd1) expressed in the frontal cortex and renin (Ren), pancreatic polypeptide (Ppy), corticotropin releasing hormone receptor 2 (Crhr2), carbonic anhydrase 1 (Car1), and hypocretin receptor 1 (Hcrtr1) expressed in the hypothalamus. We found significant differences between the expression levels of Agps and Hspb2 mRNAs in the frontal cortex and that of Ppy, Crhr2 mRNAs in the hypothalamus in the presence of high concentrations of CO2. Further investigation of these genes may clarify the pathophysiology of acute CO2 poisoning and facilitate the development of novel forensic tests that can diagnose the cause of death.
Journal: Legal Medicine - Volume 19, March 2016, Pages 101–106