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Darrren T. Lerner

Publications and source records attributed to Darrren T. Lerner.

5 recordsLinked to original sources

Evidence for episodic acidification effects on migrating Atlantic salmon Salmo salar smolts

Field studies were conducted to determine levels of gill aluminium as an index of acidification effects on migrating Atlantic salmon Salmo salar smolts in the north-eastern U.S.A. along mainstem river migration corridors in several major river basins. Smolts emigrating from the Connecticut River, where most (but not all) tributaries were well buffered, had low or undetectable levels of gill aluminium and high gill Na + /K + -ATPase (NKA) activity. In contrast, smolts emigrating from the upper Merrimack River basin where most tributaries are characterized by low pH and high inorganic aluminium had consistently elevated gill aluminium and lower gill NKA activity, which may explain the low adult return rates of S. salar stocked into the upper Merrimack catchment. In the Sheepscot, Narraguagus and Penobscot Rivers in Maine, river and year-specific effects on gill aluminium were detected that appeared to be driven by underlying geology and high spring discharge. The results indicate that episodic acidification is affecting S. salar smolts in poorly buffered streams in New England and may help explain variation in S. salar survival and abundance among rivers and among years, with implications for the conservation and recovery of S. salar in the north-eastern U.S.A. These results suggest that the physiological condition of outmigrating smolts may serve as a large-scale sentinel of landscape-level recovery of atmospheric pollution in this and other parts of the North Atlantic region.

Journal of Fish Biology↗

Thresholds for short-term acid and aluminum impacts on Atlantic salmon smolts

Although the negative effects of acid and aluminum (Al) on smolt development have been known for some time, the thresholds for impact of short-term exposure of several days that may occur during episodic acidification have not been systematically examined. In order to determine the levels of acid and Al that impact juvenile Atlantic salmon, smolts and yolk-sac larvae were exposed to three pH levels (6.0, 5.7, and 5.3) and four added Al levels (0, 40, 80 and 175 μg/L total Al) for 48 h. Following this treatment, 10 smolts were sampled in freshwater and another 10 were subjected to a 24 h seawater challenge (35 ppt). Survival of yolk-sac larvae was > 96% in all acid and Al treatments. All smolts died within 48 h at pH 5.3, 175 μg L− 1 Al. There were some mortalities in freshwater at pH 5.3, 80 μg L− 1 Al and pH 5.7, 175 μg L− 1 Al, and further mortalities when these fish were transferred to seawater. Mortalities in these groups were associated with decreased plasma chloride in freshwater and higher plasma chloride in seawater, indicating that these smolts had lost seawater tolerance. Gill Na+/K+-ATPase (NKA) activity decreased at pH 5.7, 175 μg L− 1 Al in freshwater, and further decreases were observed at more moderate pH and Al exposures after transfer to seawater. Hematocrit and plasma glucose were the most sensitive physiological responses, increasing at all Al treatments at pH 5.7 and 5.3 in freshwater. There was no detectable increase in gill Al levels at pH 6.0 with added Al, whereas substantial increases in gill Al were observed in all added Al groups at pH 5.7 and 5.3. Our results demonstrate a critical interaction between acid and Al in their effects on smolts, and that episodic acidification events will negatively impact smolt survival in freshwater and after seawater entry.

Aquaculture↗

Aqueous exposure to 4-nonylphenol and 17β-estradiol increases stress sensitivity and disrupts ion regulatory ability of juvenile atlantic salmon

Population declines of wild Atlantic salmon have been attributed to an array of anthropogenic disturbances, including dams, commercial and recreational fishing, habitat loss, and pollution. Environmental contaminants in particular, can act as environmental stressors on fish, typically causing disruption of ion homeostasis due to their close association with the aquatic environment. To examine the effects of the xenoestrogen 4-nonylphenol (NP) or 17β-estradiol (E 2 ) on stress sensitivity and ion regulation, we exposed juvenile Atlantic salmon continuously for 21 d to either 10 or 100 μg/L NP (NP-L or NP-H), 2 μg/L E 2 (positive control), or vehicle control during the parr-smolt transformation in April. After treatment, fish were sampled in freshwater (FW), transferred to 30‰ seawater (SW) for 24 h, or subjected to a handling stress. Estradiol and NP-H increased plasma vitellogenin in males and females, and E 2 increased gonadosomatic index only in males. In FW, E 2 reduced sodium potassium–activated adenosine triphosphatase activity as well as plasma levels of growth hormone, insulin-like growth factor I, and triiodothyronine. Both E 2 and NP-H reduced plasma sodium in FW and increased plasma chloride in SW. Plasma Cortisol levels pre- and poststressor were significantly elevated by all treatments relative to controls, but only E 2 increased plasma glucose before and after the stressor. These results indicate that exposure of anadromous salmonids to environmental estrogens heightens sensitivity to external stressors, impairs ion regulation in both FW and SW, and disrupts endocrine pathways critical for smolt development.

Environmental Toxicology and Chemistry↗

Larval exposure to 4-nonylphenol and 17β-estradiol affects physiological and behavioral development of seawater adaptation in Atlantic salmon smolts

Population declines of anadromous salmonids are attributed to anthropogenic disturbances including dams, commercial and recreational fisheries, and pollutants, such as estrogenic compounds. Nonylphenol (NP), a xenoestrogen, is widespread in the aquatic environment due to its use in agricultural, industrial, and household products. We exposed Atlantic salmon yolk-sac larvae to waterborne 10 or 100 μg L -1 NP (NP-L or NP-H, respectively), 2 μg L -1 17β-estradiol (E 2 ), or vehicle, for 21 days to investigate their effects on smolt physiology and behavior 1 year later. NP-H caused approximately 50% mortality during exposure, 30 days after exposure, and 60 days after exposure. Mortality rates of NP-L and E 2 fish were not affected until 60 days after treatment, when they were 4-fold greater than those of controls. Treatment with NP-L or E 2 as yolk-sac larvae decreased gill sodium-potassium-activated adenosine triphosphatase (Na + ,K + -ATPase) activity and seawater (SW) tolerance during smolt development, 1 year after exposure. Exposure to NP-L and E 2 resulted in a latency to enter SW and reduced preference for SW approximately 2- and 5-fold, respectively. NP-L-exposed fish had 20% lower plasma insulin-like growth factor I (IGF-I) levels and 35% lower plasma triiodothyronine (T 3 ). Plasma growth hormone and thyroxine (T 4 ) were unaffected. Exposure to E 2 did not affect plasma levels of IGF-I, GH, T 3 , or T 4 . Both treatment groups exhibited increased plasma cortisol and decreased osmoregulatory capacity in response to a handling stressor. These results suggest that early exposure to environmentally relevant concentrations of NP, and other estrogenic compounds, can cause direct and delayed mortalities and that this exposure can have long term, “organizational” effects on life-history events in salmonids.

Environmental Science & Technology↗

Endocrine disruption of parr-smolt transformation and seawater tolerance of Atlantic salmon by 4-nonylphenol and 17β-estradiol

Sex steroids are known to interfere with the parr-smolt transformation of anadromous salmonids, and environmental estrogens such as nonylphenol have recently been implicated in reduced returns of Atlantic salmon in the wild. To determine the endocrine pathways by which estrogenic compounds affect smolt development and seawater tolerance, groups of juvenile Atlantic salmon were injected with one of five doses (0.5, 2, 10, 40 or 150 μg g −1 ) of branched 4-nonylphenol (NP), 2 μg g −1 of 17β- estradiol (E 2 ), or vehicle, during the parr-smolt transformation in April, and the treatment was repeated 4, 8, and 11 days after the first injection. Plasma was obtained for biochemical analysis 7 and 14 days after initiation of treatment. After 14 days of treatment, additional fish from each treatment group were exposed to seawater for 24 h to assess salinity tolerance. The E 2 treatment and the highest NP dose resulted in lower salinity tolerance and decreased plasma insulin-like growth factor I (IGF-I) levels, along with elevated levels of plasma vitellogenin and total calcium. Plasma growth hormone levels were elevated at intermediate NP doses only, and not affected by E 2 . After 7 days, plasma thyroxine (T 4 ) levels decreased in a strong, dose-dependent manner in response to nonylphenol, but after 14 days, this suppressive effect of T 4 occurred at the highest NP dose only. Similarly, E 2 decreased plasma T 4 levels at 7, but not 14 days. Plasma 3,3′,5-triodo- l -thyronine was reduced by E 2 and the highest NP dose after 7 and 14 days of treatment. Plasma cortisol levels were not affected by any of the treatments. The results indicate that the parr-smolt transformation and salinity tolerance can be compromised by exposure to estrogenic compounds. Suppression of plasma IGF-I levels is a likely endocrine pathway for the effects of estrogenic compounds on hypo-osmoregulatory capacity, and the detrimental effects of E 2 and NP on thyroid hormone levels are also likely to compromise the normal parr-smolt transformation of Atlantic salmon.

General and Comparative Endocrinology↗