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. 2016 Apr 19:4:e1956.
doi: 10.7717/peerj.1956. eCollection 2016.

Changes to coral health and metabolic activity under oxygen deprivation

James W A Murphy  1 , Robert H Richmond  1
Affiliations

Changes to coral health and metabolic activity under oxygen deprivation

James W A Murphy et al. PeerJ. .

Abstract

On Hawaiian reefs, the fast-growing, invasive algae Gracilaria salicornia overgrows coral heads, restricting water flow and light, thereby smothering corals. Field data shows hypoxic conditions (dissolved oxygen (DO2) < 2 mg/L) occurring underneath algal mats at night, and concurrent bleaching and partial tissue loss of shaded corals. To analyze the impact of nighttime oxygen-deprivation on coral health, this study evaluated changes in coral metabolism through the exposure of corals to chronic hypoxic conditions and subsequent analyses of lactate, octopine, alanopine, and strombine dehydrogenase activities, critical enzymes employed through anaerobic respiration. Following treatments, lactate and octopine dehydrogenase activities were found to have no significant response in activities with treatment and time. However, corals subjected to chronic nighttime hypoxia were found to exhibit significant increases in alanopine dehydrogenase activity after three days of exposure and strombine dehydrogenase activity starting after one overnight exposure cycle. These findings provide new insights into coral metabolic shifts in extremely low-oxygen environments and point to ADH and SDH assays as tools for quantifying the impact of hypoxia on coral health.

Keywords: Alanopine dehydrogenase; Anoxia; Coral metabolism; Corals; Ecological resilience; Enzyme activity; Hawaii; Hypoxia; Montipora capitata; Strombine dehydrogenase.

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Conflict of interest statement

The authors declare there are no competing interests.

Figures

Figure 1
Figure 1. Typical cellular respiration pathway in eukaryotic cells.
Red box denotes anaerobic respiratory pathway of interest.
Figure 2
Figure 2. Pyruvate metabolism pathways.
Conversion of pyruvate to lactate by lactate dehydrogenase (LDH, 1), pyruvate and alanine to alaopine by alanopine dehydrogenase (ADH, 2), pyruvate and arginine to octopine by octopine dehydrogenase (ODH, 3), and pyruvate and glycine to strombine by strombine dehydrogenase (SDH, 4).
Figure 3
Figure 3. Sampling scheme displaying collections over treatment period (blue signifying overnight bubbling and yellow, the return to normal oxygen levels during the day).
Arrow 1 corresponds to the ‘3 h’ collection time point, 2 to ‘6 h,’ 3 to ‘1 day,’ and 4 to ‘3 days.’ ‘Day 5’ of bubbling was omitted, as tissue loss rendered those samples unsuitable for analysis.
Figure 4
Figure 4. Lactate dehydrogenase (LDH) activity (nmols/min/mg pro) versus treatment time and type (3, 6 h and 1, 3 days).
Bars represent mean ± SD.
Figure 5
Figure 5. Octopine dehydrogenase (ODH) activity (nmols/min/mg prot) versus treatment time and type (3, 6 h and 1, 3 days).
Bars represent mean ± SD.
Figure 6
Figure 6. Strombine dehydrogenase (SDH) activity (nmols/min/mg prot) versus treatment time and type (3, 6 h and 1, 3 days).
Bars represent mean ± SD. Treatments with significantly higher SDH activity than controls are denoted in treatments marked with asterisks (∗, p < 0.05; ∗∗∗, p < 0.001)
Figure 7
Figure 7. Alanopine dehydrogenase (ADH) activity (nmols/min/mg prot) versus treatment time and type (3, 6 h and 1, 3 days).
Bars represent mean ± SD. The 3 day treatment with significantly higher ADH activity than controls is denoted by an asterisk (∗∗, p < 0.01).
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