Literature DB >> 17353058

Physiological effects of polycyclic aromatic hydrocarbons on soft-shell clam Mya arenaria.

H Frouin1, J Pellerin, M Fournier, E Pelletier, P Richard, N Pichaud, C Rouleau, F Garnerot.   

Abstract

The aim of this study was to investigate the effects of polycyclic aromatic hydrocarbons (PAHs) on the physiological status of the bivalve Mya arenaria. Specimens were exposed to four different sources of PAHs: aluminium smelter soot, sediment from an industrial discharge pound, charcoal fine particles and dietary PAHs assessed by feeding clams with phytoplankton freshly impregnated with dissolved PAHs. The exposure period lasted 30 days and bivalves were let to recover for an additional 20 days. At days 8, 15, 30 and 50, immune parameters (phagocytic activity and efficiency) were monitored in haemocytes. Oxidative stress measures such as catalase and lipid peroxidation were quantified in digestive gland as well as concentrations of bioaccumulated PAHs. In a second experiment, clams were exposed to [(14)C]-pyrene via the phytoplankton, and the tissue distribution of radiolabelled compound was studied. Glycogen levels in gonad and digestive gland were also measured and gametogenesis stages were investigated. Results showed a high bioaccumulation in clams exposed to dietary PAHs and contaminated sediments. Tissue distribution of [(14)C]-pyrene revealed that the radiolabelled compound persisted mainly in the gonad during 14 days. A decrease of phagocytosis was observed in contaminated male clams. The lipid peroxidation (malondialdehyde) was found to increase in the digestive gland tissues of clams exposed to dietary PAHs, smelter soot and discharge, but no differences were observed in the catalase activity. A delay in gametogenesis occurred in all exposed males and in females contaminated with coke dust and dietary PAHs. Males were more sensitive than females to PAH exposure. A dysfunction in steroid synthesis is suspected to occur due to the exposure to all sources of PAHs.

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Year:  2007        PMID: 17353058     DOI: 10.1016/j.aquatox.2007.02.005

Source DB:  PubMed          Journal:  Aquat Toxicol        ISSN: 0166-445X            Impact factor:   4.964


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