The effect of hypercapnic hypoxia and bacterial infection on protein synthesis rates in the Pacific whiteleg shrimp, Litopenaeus vannamei


Meeting Abstract

P1.58  Wednesday, Jan. 4  The effect of hypercapnic hypoxia and bacterial infection on protein synthesis rates in the Pacific whiteleg shrimp, Litopenaeus vannamei HARDY, KM*; BURNETT, KG; BURNETT, LE; Cal Poly State Univ – San Luis Obispo; Medical Univ of South Carolina; College of Charleston; College of Charleston kmhardy@calpoly.edu

Estuarine species frequently encounter areas of low dissolved O2 (hypoxia; H) and high CO2 (hypercapnia; HH). Exposure to low O2 results in a downregulation of metabolic rate that serves to decrease ATP utilization and O2 demand. This depression is facilitated by a reduction in protein synthesis, which can be responsible for up to 60% of total basal metabolism. We have previously observed a decrease in the relative mRNA levels of genes involved in protein synthesis during H and HH in the Pacific whiteleg shrimp, Litopenaeus vannamei. In the present study, we aimed to confirm that this hypoxia-induced metabolic downregulation is accompanied by a decrease in protein synthesis. Metabolic depression has also been observed in other decapods in response to bacterial challenge, leading us to hypothesize that protein synthesis may also be reduced during infection. Here we examined the effects of H, HH and bacterial infection (Vibrio campbellii) on tissue-specific [muscle and hepatopancreas (Hp)] total protein synthesis rates (Ks) in L. vannamei, as determined by the rate of tissue incorporation of radiolabeled [3H]-phenylalanine. We observed a significant decrease in Ks in muscle after 24h exposure to both H and HH, and in Hp after 4 and 24h exposure to HH. Thus, in Hp tissue the combined stress of H and hypercapnia exacerbated their effect on Ks. Bacterial infection (24h), however, had no significant effect on Ks in either tissue. These results suggest that marine crustaceans reduce metabolic demand during environmental hypercapnic hypoxia by reducing global protein synthesis, whereas this mechanism does not seem to facilitate decreased metabolic rates associated with infection.

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