Abstract

The Manila clam Ruditapes philippinarum has become a common and dominant macrobenthic species in coastal areas of the northwestern Pacific and temperate waters of Europe; it is also a major cultured shellfish, with annual worldwide production exceeding 3.3 million tonnes. This species faces greater risk of exposure to hypoxia as eutrophication worsens throughout its coastal habitats; however, its tolerance to hypoxia remains unclear, and the toxicological indicators including LC50 and LT50 have not yet been assessed. Previous studies on the effects of hypoxia on marine benthos have focused largely on functional responses, such as metabolism and gene expression, leaving potential structural damage to the mitochondria or the cells unknown. In this study we assessed the effects of hypoxia on Manila clam in terms of survival, behavior, metabolism and cellular damage, using a newly designed automated hypoxia simulation device that features exceptional accuracy and good stability. The clams exhibited strong tolerance to hypoxia as the 20-day LC50 for dissolved oxygen (DO) was estimated to be 0.57 mg L-1, and the LT50 at 0.5 mg L-1 DO was 422 hours. Adaptations included fewer buried clams and a depressed metabolism, while the unexpected rise in the activities of key enzymes involved in glycolysis may indicate a diverse strategy of shellfish under hypoxia. Cellular damage was observed as collapse of the mitochondrial cristae and both cellular and mitochondrial vacuolization. This multi-level study complements and updates our knowledge of the effects of hypoxia on marine benthos, by improving our understanding of the potential for marine ecological transformation under hypoxic conditions and providing useful information for Manila clam farming.

Highlights

  • As the eutrophication of coastal waters intensifies, both the extent and strength of oxygen depletion increase [1,2]

  • During the 3 to 5 days, a few of the clams exposed to 0.5 mg L-1 dissolved oxygen (DO) began to die at a slow rate, followed by deaths among those exposed to 1.0 mg L-1 DO

  • The LT50 at 0.5 mg L-1 DO was calculated as 422 hours, and the 20-day LC50 was estimated to be 0.57 mg L-1 DO when the experiments using more DO concentrations were conducted as part of Experiment 2

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Summary

Introduction

As the eutrophication of coastal waters intensifies, both the extent and strength of oxygen depletion (hypoxia) increase [1,2]. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript

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