41 resultados para SL


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Individuals of Mytilus edulis L., collected from the Erme estuary (S.W. England) in 1978, were exposed to low concentrations (7 to 68 μg l-1) of the water-accommodated fraction (WAF) of North Sea crude oil. The pattern of accumulation of petroleum hydrocarbons in the body tissues was affected by the presence of algal food cells, the period of exposure, the hydrocarbon concentration in seawater, the type of body tissue and the nature of the hydrocarbon. Many physiological responses (e.g. rates of oxygen consumption, feeding, excretion, and scope for growth), cellular responses (e.g. lysosomal latency and digestive cell size) and biochemical responses (e.g. specific activities of several enzymes) were significantly altered by short-term (4 wk) and/or long-term (5 mo) exposure to WAF. Stress indices such as scope for growth and lysosomal latency were negatively correlated with tissue aromatic hydrocarbons.

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The population dynamics of Mytilicola intestinalis Steuer in mussels (Mytilus edulis L.) from the River Lynher, Cornwall, England, have been studied over 3 years. By transplanting uninfested mussels from the River Erme, South Devon, into the Lynher mussel bed, the study was extended to the growth and development of new infestations under natural conditions. Female Mytilicola intestinalis are shown to breed twice, and two generations of parasites coexist for most of the year, with recruitment taking place in summer and autumn. One generation contributes its first brood to the autumn recruits before overwintering and contributing its second brood to the following summer's recruits. The other generation overwinters as juvenile and immature stages to contribute its two broods successively to the summer and autumn recruits. Environmental temperatures are believed to control the rates of development at all stages rather than acting as triggers in the onset or cessation of breeding at specific times. There is no evidence to support the contention that heavily infested mussels are killed, and parasite mortality is shown to be density-independent.