Chronic effects of dietary selenium on juvenile Sacramento splittail (Pogonichthys macrolepidotus).
The chronic effects of dietary selenium (Se) exposure in juvenile Sacramento splittail (Pogonichthys macrolepidotus) were investigated in the laboratory. A total of 960 (40 fish per tank, 3 tanks per diet) 7-month-old juvenile splittail were fed one of eight Purified-Casein diets supplemented with selenized yeast for 9 months in a flow-through system. These diets contained the following: 0.4 (control), 0.7, 1.4, 2.7, 6.6, 12.6, 26.0, and 57.6 mg of Se kg(-1) dry weight. Survival, Se tissue concentration, growth, gross morphology, and liver histopathology were assessed at 5- and 9-month of exposure. Mortalities occurred only in the two highest Se treatments and were accounted for 8.3 and 18.3% at 5-month and 10.0 and 34.3% at 9-month, respectively. Liver and muscle Se concentration were significantly correlated with dietary Se concentration. Fish exposed to 0.4-12.6 mg of Se kg(-1) diets had reached equilibrium in liver Se concentration by 5 month. Splittail fed diets at concentrations > or =26.0 mg of Se kg(-1) had not reached equilibrium in liver, and muscle Se concentrations and grew significantly slower (p < 0.05) at 5- and 9-month exposure. Se-induced deformities were observed in fish fed > or =2.7 mg of Se kg(-1) diets at 5-month and in fish fed > or =0.7 mg of Se kg(-1) diets at 9-month. Fish fed 26.0 and 57.6 mg of Se kg(-1) diets had higher liver lesion scores at 5-month while fish fed 6.6 and 57.6 mg of Se kg(-1) diet had higher liver lesion scores at 9-month. Results indicate that survivals, growth, changes of tissue Se concentrations, and histopathology of juvenile splittail were dose-dependent, but their response thresholds to dietary Se concentrations differed and depended on treatment concentrations and duration of exposure. Chronic exposure to 6.6 mg of Se kg(-1) diet induced deleterious health effects that can potentially impact survival of juvenile splittail.
Teh
Swee J
SJ
Aquatic Toxicology Program, Department of Anatomy, Physiology, and Cell Biology, School of Veterinary Medicine, University of California, Davis, California 95616, USA. sjteh@ucdavis.edu
Deng
Xin
X
Deng
Dong-Fang
DF
Teh
Foo-Ching
FC
Hung
Silas S O
SS
Fan
Teresa W M
TW
Liu
Jee
J
Higashi
Richard M
RM
D000818:Animals; D003530:Cyprinidae / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004781:Environmental Exposure; D005393:Fish Diseases / Q000139:chemically induced; D006128:Growth / Q000187:drug effects; D008099:Liver / Q000378:metabolism / Q000473:pathology; D008141:Lordosis / Q000139:chemically induced / Q000662:veterinary; D018482:Muscle, Skeletal / Q000378:metabolism; D012600:Scoliosis / Q000139:chemically induced / Q000662:veterinary; D012643:Selenium / Q000008:administration & dosage / Q000633:toxicity*; D016019:Survival Analysis; D013997:Time Factors; D014018:Tissue Distribution; D014874:Water Pollutants, Chemical / Q000008:administration & dosage / Q000633:toxicity*
D014874:Water Pollutants, Chemical; D012643:Selenium