Decreased growth and survival in small juvenile fish, after chronic exposure to environmentally relevant concentrations of microplastic

2019 ◽  
Vol 145 ◽  
pp. 254-259 ◽  
Author(s):  
Trishan Naidoo ◽  
David Glassom
2013 ◽  
Vol 3 (11) ◽  
pp. 3855-3867 ◽  
Author(s):  
John R. Morrongiello ◽  
Nicholas R. Bond ◽  
David A. Crook ◽  
Bob B. M. Wong

1985 ◽  
Vol 42 (12) ◽  
pp. 1986-1993 ◽  
Author(s):  
S. M. Bower ◽  
L. Margolis ◽  
R. J. MacKay

Susceptibility to the lethal effects of low levels of total residual chlorine (TRC) differed between juvenile coho salmon (Oncorhynchus kisutch) and the salmon leech (Piscicola salmositica), the vector for the haemoflagellate salmonid pathogen Cryptobia salmositica. There was no salmon mortality at concentrations below approximately 50 μg TRC/L for the maximum exposure time of 24 h. Some damage to gill tissue (hypertrophy, fusion, oedema, and some necrosis), was observed at the highest concentrations of TRC that did not kill any of the fish (approximately 50 μg/L for 24 h, and approximately 100 μg/L for 8 h). This damage was repaired by the fish within 4 d of exposure, although evidence of past irritation was noted in 6 of 12 fish. All small juvenile leeches exposed to 44 μg TRC/L for 24 h died, and over half of such leeches exposed to 44 μg/L for 8 h and 21 μg/L for 24 h died. Below TRC concentrations that were lethal to the fish (approximately 50 μg/L), contours of constant leech mortality derived from a logistic regression model fitted to the data offered a wide range of concentrations and exposure times that would result in high mortality of juvenile leeches. Larger subadult and adult leeches were more resistant to chlorine than the smaller leeches but were more sensitive than the juvenile fish. Thus, chlorine may prove useful for controlling P. salmositica in salmonid hatcheries.


2014 ◽  
Vol 26 (2) ◽  
pp. 106-110 ◽  
Author(s):  
Li JunFeng ◽  
Wang Wei ◽  
Zhang Saisai ◽  
Wang Hua ◽  
Xie Huan ◽  
...  

1993 ◽  
Vol 1 (2) ◽  
pp. 172-197 ◽  
Author(s):  
P. M. Outridge ◽  
A. M. Scheuhammer

The tissues of wild mammals and birds from uncontaminated environments generally contain from ~0.1 to 5 μg nickel∙g dry weight−1, whereas in Ni-polluted environments, tissues accumulate from -0.5 to 10 (mammals) and -0.5 to 80 (birds) μg nickel∙g dry weight−1. The highest concentrations in these ranges are usually associated with tissues directly exposed to the external environment (fur, feathers, skin). Bone frequently contains higher Ni concentrations than other internal tissues. Ni concentrations in the most commonly analysed internal organs (liver, kidneys) range from nondetectable to about 3 μg∙g dry weight−1, the kidneys often containing higher concentrations than the liver. There is some evidence that birds may tend to accumulate higher Ni burdens in polluted habitats than do mammals. For mammals, reduced growth and survival occur in response to chronic exposure to 500–2500 μg Ni∙g diet−1 (10–50 mg∙kg body weight−1∙d−1). Effects on reproduction and essential trace metal (especially iron) metabolism have been reported at levels as low as 5 μg∙g−1 in food or drinking water (0.2–0.4 mg∙kg body weight−1∙d−1), but these findings have not always been corroborated. Toxicological data on birds are more limited than those pertaining to mammals. Newly hatched chickens suffered reduced growth rates when fed ≥300 μg∙g diet−1, and chicks began to die when fed diets containing ≥500 μg∙g−1. In newly hatched mallard ducklings, chronic exposure to ≥800 μg∙g diet−1 resulted in ataxia, tremors, and significant mortality, whereas adult mallards fed 800 μg∙g−1 showed no evidence of systemic or reproductive toxicity. Tissue concentrations of Ni were not reliable indicators of potential toxicity in either mammals or birds, because significant effects, including mortality, frequently occurred in the absence of elevated tissue Ni concentrations. However, when there is evidence of elevated tissue Ni concentrations (>10 μg∙g−1 in the kidneys, and (or) >3 μg∙g−1 dry weight in the liver), Ni exposure sufficient to cause significant toxic effects should be suspected. Nickel has been reported in aquatic macrophytes and lower plants (but not in invertebrates or zooplankton) in the vicinity of Ni smelters in Canada in concentrations that approach or exceed dietary levels known to cause adverse effects in young animals. Sensitive species of wildlife ingesting this vegetation for considerable periods of time could experience Ni-related toxicity. In addition, wildlife food chains involving aquatic organisms (plants, invertebrates, fish) risk alterations in community structure in Ni-contaminated environments as Ni-sensitive taxa are eliminated or their abundance is reduced.Key words: nickel, toxicology, wildlife.


2019 ◽  
Author(s):  
Jacqueline Weidner ◽  
Camilla Håkonsrud Jensen ◽  
Jarl Giske ◽  
Sigrunn Eliassen ◽  
Christian Jørgensen

AbstractGrowth is an important theme in many biological disciplines. Physiologists often relate growth rates to hormonal control of essential processes. Ecologists often study growth as function of gradients or combinations of environmental factors. Fewer studies have investigated the combined effects of environmental and hormonal control on growth. Here, we present an evolutionary optimization model of fish growth that combines internal regulation of growth by hormone levels with the external influence of food availability and predation risk. Hormones are represented by growth hormone, thyroid hormone and orexin functions. By studying a range from poor to rich environments, we find that the level of food availability in the environment results in different evolutionarily optimal strategies of hormone levels. With more food available, higher levels of hormones are optimal, resulting in higher food uptake and growth. By using this fitness-based approach we also find a consequence of evolutionary optimization of survival on optimal hormone use. Where foraging is risky, aerobic scope can be used strategically to increase the chance of escaping from predators. By comparing model results to empirical observations, many mechanisms can be recognized, for instance a change in pace-of-life due to resource availability, and reduced emphasis on reserves in more stable environments.Summary statementWe combine physiological, environmental and evolutionary aspects of fish growth in a state-dependent model where the optimal regulation of growth and survival is achieved through hormonal regulation of behaviour.


Oikos ◽  
2020 ◽  
Vol 130 (1) ◽  
pp. 41-51
Author(s):  
Camilla Håkonsrud Jensen ◽  
Jacqueline Weidner ◽  
Jarl Giske ◽  
Sergey Budaev ◽  
Christian Jørgensen ◽  
...  

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