Recovery from hypoxia and hypercapnic hypoxia Impacts on the transcription of key antioxidant genes in the shrimp Litopenaeus vannamei


Meeting Abstract

80.2  Friday, Jan. 6  Recovery from hypoxia and hypercapnic hypoxia: Impacts on the transcription of key antioxidant genes in the shrimp Litopenaeus vannamei. DARLING, CL*; BURNETT, LE; BURNETT, KG; College of Charleston; College of Charleston; College of Charleston darlingcl@gmail.com

The Pacific whiteleg shrimp, Litopenaeus vannamei, inhabits coastal estuarine waters which are prone to intermittent bouts of low oxygen (hypoxia) and high carbon dioxide (hypercapnia) followed by a return, or recovery, to fully air-saturated levels of oxygen and carbon dioxide (normoxia). Hypoxia (H) and hypercapnic hypoxia (HH) can cause oxidative stress which induces production of reactive oxygen species (ROS) that damage surrounding cells and tissues. In vertebrates, sudden rises in oxygen levels also increase ROS production. Cellular production of antioxidants, which convert ROS into non-toxic molecules, can prevent cell damage. Here we examine antioxidant production in the hepatopancreas of L.vannamei after recovery from H or HH. Prior studies revealed that transcription of antioxidants thioredoxin-2 (TRX-2) and glutathione-s-transferase (GST) was significantly upregulated (2.7; 2.9-fold, respectively) after 4 h exposure to H. Only GST was significantly upregulated (3.9-fold) after 4 h in HH; neither antioxidant was upregulated after 24 h in H or HH. In the current study we exposed shrimp to H or HH for 4 or 24 h. Shrimp subsequently recovered in normoxia for 1, 6, or 24 h. Transcriptional changes of TRX-2, GST, and other antioxidant-related genes are currently being quantified by qRT-PCR. Based on prior studies detailed above, we expect that transcription of antioxidant-related genes will further increase in response to increases in oxygen during recovery from 4 h H or HH, but that this increase will not occur during recovery from 24 h H or HH, leaving these animals susceptible to oxidative damage as tissue oxygenation returns to normal levels.

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