Salmon toxicity
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Salmon Toxicity: An Overview of Recent Research
Uranium Toxicity in Atlantic Salmon
Chemical Toxicity and Gene Expression
Uranium (U) exposure in Atlantic salmon (Salmo salar) has been shown to cause significant changes in gene expression. When exposed to depleted uranium (DU) at concentrations of 0.25, 0.5, and 1.0 mg U/L for 48 hours, salmon exhibited differential expression of hundreds of genes associated with energy metabolism, carbohydrate processes, and cellular homeostasis. The primary toxicological mechanisms identified include mitochondrial dysfunction and oxidative stress, which can lead to apoptosis, DNA repair, hypoxia signaling, and immune responses1.
6PPD-Quinone Toxicity in Salmon Species
Acute Toxicity in Juvenile Chinook and Coho Salmon
The breakdown product of the rubber tire antioxidant 6PPD, known as 6PPD-quinone, has been found to be highly toxic to coho salmon (Oncorhynchus kisutch) and Chinook salmon (Oncorhynchus tshawytscha). Juvenile coho salmon are particularly sensitive, with a 24-hour median lethal concentration (LC50) of 41.0 ng/L, whereas juvenile Chinook salmon have a much higher LC50 of over 67,307 ng/L. Symptoms of exposure include gasping, increased ventilation, loss of equilibrium, and erratic swimming, often leading to mortality2.
Toxicity in Atlantic Salmon and Brown Trout
In contrast, Atlantic salmon (Salmo salar) and brown trout (Salmo trutta) alevins showed no significant mortality or behavioral changes when exposed to 6PPD-quinone concentrations ranging from 0.095 to 12.16 µg/L over 48 hours. This suggests species-specific differences in sensitivity to this contaminant, complicating environmental risk assessments4.
Paralytic Shellfish Toxins (PSTs) in Salmon
Impact of Alexandrium Blooms
Blooms of the dinoflagellate Alexandrium fundyense, which produce paralytic shellfish toxins (PSTs), have been linked to significant mortalities in caged Atlantic salmon. During a bloom in the Bay of Fundy, high concentrations of PSTs were detected in zooplankton and mussels, which are part of the salmon's diet. The toxins were found in the gills of affected salmon, indicating that direct exposure to toxic Alexandrium cells or soluble toxins was the likely cause of mortality3 7.
Metabolic Response to PSTs
Exposure to PSTs induces the activity of xenobiotic metabolizing enzymes (XMEs) such as cytochrome P-450 (CYP1A) and glutathione S-transferase (GST) in Atlantic salmon. This enzymatic response suggests a potential role for XMEs in the metabolism and detoxification of PSTs, although the exact mechanisms remain to be fully understood6.
Heavy Metal Toxicity in Salmon
Cadmium, Copper, and Zinc
Acute toxicity tests have shown that adult male coho salmon and steelhead (Salmo gairdneri) are susceptible to heavy metals such as cadmium, copper, and zinc. The 96-hour LC50 values for copper were 46 µg/L for coho salmon and 57 µg/L for steelhead, while zinc LC50 values were 905 µg/L and 1,755 µg/L, respectively. Cadmium induced mortality more slowly, with 50% mortality occurring at 3.7 µg/L for coho salmon and 5.2 µg/L for steelhead5.
Conclusion
The research highlights the diverse toxicological threats faced by salmon species, ranging from chemical contaminants like uranium and 6PPD-quinone to natural toxins produced by algal blooms and heavy metals. Understanding these toxicological mechanisms and species-specific responses is crucial for developing effective conservation and management strategies to protect these vital aquatic organisms.
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Most relevant research papers on this topic
Hepatic transcriptomic profiling reveals early toxicological mechanisms of uranium in Atlantic salmon (Salmo salar)
Uranium toxicity in Atlantic salmon involves mitochondrial dysfunction, oxidative stress, and organ damage, but no other physiological changes were observed.
Acute Toxicity of 6PPD‐Quinone to Early Life Stage Juvenile Chinook (Oncorhynchus tshawytscha) and Coho (Oncorhynchus kisutch) Salmon
6PPD-quinone is acutely toxic to juvenile Chinook and coho salmon, with coho being more sensitive, suggesting potential population-level consequences in urban waterways.
Paralytic shellfish toxins in zooplankton, mussels, lobsters and caged Atlantic salmon, Salmo salar, during a bloom of Alexandrium fundyense off Grand Manan Island, in the Bay of Fundy
A bloom of Alexandrium fundyense in the Bay of Fundy led to high paralytic shellfish toxin levels in zooplankton, mussels, and lobsters, causing significant mortality in Atlantic salmon aquaculture.
Acute Toxicity Testing of the Tire Rubber–Derived Chemical 6PPD‐quinone on Atlantic Salmon (Salmo salar) and Brown Trout (Salmo trutta)
6PPD-quinone does not cause mortalities or significant behavioral changes in Atlantic salmon or brown trout, providing a first step in assessing its effects on these economically and culturally important species.
Acutely Lethal Levels of Cadmium, Copper, and Zinc to Adult Male Coho Salmon and Steelhead
Acute toxicity levels of cadmium, copper, and zinc are lethal to adult male coho salmon and steelhead, with cadmium mortality occurring at 3.7 and 5.2 g/liter, respectively.
Paralytic shellfish poisoning toxins induce xenobiotic metabolising enzymes in Atlantic salmon (Salmo salar).
Induction of xenobiotic metabolising enzymes in Atlantic salmon suggests a potential role for XMEs in paralytic shellfish poisoning toxin metabolism.
The toxigenic marine dinoflagellate Alexandrium tamarense as the probable cause of mortality of caged salmon in Nova Scotia
A massive bloom of the marine dinoflagellate Alexandrium tamarense in 2000 led to high mortality of caged salmon in Nova Scotia, likely due to direct exposure to toxic cells and soluble toxins released during the bloom.
Swimming and ammonia toxicity in salmonids: the effect of sub lethal ammonia exposure on the swimming performance of coho salmon and the acute toxicity of ammonia in swimming and resting rainbow trout.
Swimming reduces ammonia toxicity in coho salmon and rainbow trout, with metabolic challenges and depolarization of white muscle causing reduced performance.
Chronic oral DDT toxicity in juvenile Coho and Chinook salmon.
Chronic oral DDT toxicity in juvenile Coho and Chinook salmon is more severe than technical DDT mixture, with chinook salmon being more sensitive and smaller, younger fish being more susceptible to a given diet.
The effect of 2‐(Thiocyanomethylthio)benzothiazole on juvenile coho salmon (Oncorhynchus Kisutch): Sublethal toxicity testing
TCMTB, a wood preservative used in British Columbia's lumber industry, can reduce swimming speed and increase blood lactate levels in juvenile coho salmon, but not oxygen consumption rates.
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