Recovery from hypoxia and hypercapnic hypoxia: impacts on the transcription of key antioxidants in the shrimp Litopenaeus vannamei

Abstract

Estuarine waters are prone to regular bouts of low oxygen (hypoxia) and high carbon dioxide (hypercapnia). In vertebrates, tissue hypoxia followed by reoxygenation can generate high levels of reactive oxygen species (ROS) that exceed cellular antioxidant capacity, leading to tissue damage. Here we quantified the expression of several antioxidant genes in the hepatopancreas of Pacific whiteleg shrimp, Litopenaeus vannamei, after exposure to hypoxia or hypercapnic hypoxia for 4h or 24h followed by recovery in air-saturated water (normoxia) for 0, 1, 6 or 24h, as compared to time-matched controls maintained only in normoxia. Transcripts of cytoplasmic Mn-superoxide dismutase (cMnSOD), glutathione peroxidase (GPX) and peptide-methionine (R)-S-oxide reductase (MsrB) increased after 4h exposure to either hypoxia or hypercapnic hypoxia; these elevated transcript levels persisted longer in animals recovering from hypercapnic hypoxia than hypoxia alone. cMnSOD transcripts generally increased, but GPX, MsrB, glutathione-S-transferase (GST), and thioredoxin 1 (TRX-1) decreased or did not change in most long-term (24h) treatment-recovery groups. Thus, the transcriptional responses of several antioxidant genes during recovery from tidally-driven hypoxia and hypercapnic hypoxia decrease or are muted by more persistent exposure to these conditions, leaving L. vannamei potentially vulnerable to ROS damage during recovery.

Keywords: Antioxidant; Hypercapnic hypoxia; Hypoxia; Litopenaeus vannamei; Reactive oxygen species.