Nickel (Ni) concentrations in the environment can rise due to human industrial activities. The toxicity of waterborne
Ni to aquatic animals has been examined in a number of previous studies; however, little is known about
the impacts of elevated dietary Ni. In the present study, zebrafish were chronically fed diets containing two
concentrations of Ni [3.7 (control) and 116 μg Ni/g diet]. Ni-exposed males, but not females, were significantly
smaller (26%) compared to controls at 80 days. In addition, total egg production was decreased by 65% in the
Ni treatment at 75–78 days of the experiment. Ni was ubiquitously distributed in control animals (similar to
previous studies), and concentrations varied between tissues by 15-fold. Ni exposure resulted in modest but
significant Ni accumulation in some tissues (increases were highest in brain, vertebrae and gut; 44%, 34%
and 25%, respectively), an effect observed only at 80 days. The limited Ni accumulation may be due to (1) the
lack of an acidified stomach in zebrafish and/or (2) the efficient upregulation of Ni transport and excretion mechanisms,
as indicated by the 4.5-fold increase inwaterborne 63Ni uptake byNi-exposed fish. Eggs fromNi-exposed
adults had Ni concentrations that were 5.2-fold higher than controls. However, by 4 days post fertilization,
larvae had similar Ni concentrations as controls, demonstrating a capacity for rapid Ni depuration. Larvae from
Ni-exposed adults were also more resistant to waterborne Ni (35% increase in the 96-h LC50 over controls). In
conclusion, elevated dietary Ni significantly affected zebrafish reproduction despite only modest tissue Ni
accumulation. There were also indications of adaptation, including increased Ni uptake rates and increased Ni
tolerance of offspring from Ni-exposed adults. Ni concentrations were particularly elevated in the brain with
exposure; possible relations to growth and reproductive impacts require further study
Nickel (Ni) concentrations in the environment can rise due to human industrial activities. The toxicity of waterborne
Ni to aquatic animals has been examined in a number of previous studies; however, little is known about
the impacts of elevated dietary Ni. In the present study, zebrafish were chronically fed diets containing two
concentrations of Ni [3.7 (control) and 116 μg Ni/g diet]. Ni-exposed males, but not females, were significantly
smaller (26%) compared to controls at 80 days. In addition, total egg production was decreased by 65% in the
Ni treatment at 75–78 days of the experiment. Ni was ubiquitously distributed in control animals (similar to
previous studies), and concentrations varied between tissues by 15-fold. Ni exposure resulted in modest but
significant Ni accumulation in some tissues (increases were highest in brain, vertebrae and gut; 44%, 34%
and 25%, respectively), an effect observed only at 80 days. The limited Ni accumulation may be due to (1) the
lack of an acidified stomach in zebrafish and/or (2) the efficient upregulation of Ni transport and excretion mechanisms,
as indicated by the 4.5-fold increase inwaterborne 63Ni uptake byNi-exposed fish. Eggs fromNi-exposed
adults had Ni concentrations that were 5.2-fold higher than controls. However, by 4 days post fertilization,
larvae had similar Ni concentrations as controls, demonstrating a capacity for rapid Ni depuration. Larvae from
Ni-exposed adults were also more resistant to waterborne Ni (35% increase in the 96-h LC50 over controls). In
conclusion, elevated dietary Ni significantly affected zebrafish reproduction despite only modest tissue Ni
accumulation. There were also indications of adaptation, including increased Ni uptake rates and increased Ni
tolerance of offspring from Ni-exposed adults. Ni concentrations were particularly elevated in the brain with
exposure; possible relations to growth and reproductive impacts require further study
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