Literature DB >> 21527282

A comparative study of phenoloxidase activity in diseased and bleached colonies of the coral Acropora millepora.

C V Palmer1, J C Bythell, B L Willis.   

Abstract

In scleractinian (hard) corals, immune responses involving phenoloxidase (PO) activity are known to play a role in coral wound healing, but there have been no studies investigating their roles in mitigating either disease or bleaching in an Indo-Pacific coral. PO activity induces the release of reactive oxygen species leading to a cytotoxic cellular environment, which enhances resistance against pathogens, but is also likely to compound oxidative stress induced during bleaching. Antioxidants such as melanin, whose synthesis is activated by PO activity, and peroxidase are potentially important for mitigating the effects of oxidative stress. Therefore, PO activity was investigated in healthy and diseased colonies of Acropora millepora. PO activity levels were compared among tissues bordering white syndrome lesions (WS) and at two locations (mid and outer) at increasing distances from lesions. Equivalent locations were sampled for PO activity on visibly healthy colonies. Additionally, PO and peroxidase activity were compared between severely bleached and healthy colonies of A. millepora. Overall, PO activity of diseased colonies was significantly lower than that of healthy colonies, but with relatively higher activity at the WS lesion border. Severely bleached colonies had significantly lower PO activity than healthy colonies, and peroxidase was also lower, but not significantly. Lower PO activity in unhealthy colonies supports earlier suggestions that lower immune activity leads to increased susceptibility to disease and bleaching. Additionally, low enzyme activity levels may indicate a depletion of colony resources. Increased PO activity at lesion borders in diseased colonies confirms the relative up-regulation of a key coral immune defense in response to WS in A. millepora.
Copyright © 2011 Elsevier Ltd. All rights reserved.

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Year:  2011        PMID: 21527282     DOI: 10.1016/j.dci.2011.04.001

Source DB:  PubMed          Journal:  Dev Comp Immunol        ISSN: 0145-305X            Impact factor:   3.636


  11 in total

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