Anoxia Tolerance, Anaerobic Metabolism, and the Lack of a Mitochondrial Permeability Transition in the Ghost Shrimp, Lepidophthalmus louisianensis, Schmitt, 1935

• Main Author: Holman, Jeremy Dale
• Other Authors: Jim H. Belanger
• Format: Others
• Language: en
• Published: LSU 2006
• Subjects: Biological Sciences
• Online Access: http://etd.lsu.edu/docs/available/etd-08162006-124346/

The ghost shrimp, Lepidophthalmus louisianensis, burrows up to meters deep in oxygen-limited marine sediments along the Gulf coast. During low tides these animals are subjected to extended periods of anoxia. The main objective of this study was to assess survival under anoxia and evaluate the physiological mechanisms that underlie the anoxia tolerance of this species. I observed large specimens of L. louisianensis (>2g) having an LT₅₀ of 64 h under anoxia at 25º C. Smaller specimens (<1g) have a significantly higher LT₅₀ of 113 h under identical conditions (P<0.0001). I measured whole body lactate levels in shrimp exposed to anoxia for up to 72 h, and recorded significant accumulation of this anaerobic end product (ANOVA, P<0.001). I also measured adenylates and arginine phosphate in shrimp exposed to anoxia for up to 48 h, and after a 24-h recovery period. Adenylates were not significantly altered during the anoxia regime, and reductions in arginine phosphate occurred after 12 and 24 h, but returned to normoxic values during recovery (ANOVA, P<0.001). While reserves of arginine phosphate are used to some extent to buffer losses in ATP, substantial contribution to the maintenance of energetic status comes from the high rate of anaerobic glycolysis. Energized mitochondria isolated from ghost shrimp hepatopancreas possess a pronounced ability to take up exogenous Ca²⁺ (compared to mitochondria-free controls) as measured by following the external free Ca²⁺ concentration with the fluorogenic dye Fluo-5N. Importantly, Ca²⁺ was not released from the mitochondrial matrix at any level of exogenous Ca²⁺ tested (up to 1.0 mM, in the presence of 5 mM phosphate). Thus, Ca²⁺ does not stimulate opening of the mitochondrial permeability transition pore, which potentially could help prevent apoptotic and necrotic cell death during extended periods of anoxia. (Supported by NIH grant 1-RO1-GM0-71345-01 and by SIGMA XI GIAR).