title: Vitamin and thyroid status in arctic grayling (Thymallus arcticus) exposed to doses of 3,3',4,4'-tetrachlorobiphenyl that induce the phase I enzyme system.
abstract: Induction of phase I biotransformation enzymes is recognized as a hallmark response in fish exposed to coplanar PCBs. Depletions of vitamins A and E and disrupted thyroid hormone and glandular structure secondary to this induction have not yet been examined in an arctic fish species. Arctic grayling were exposed to a single oral dose of 0 (control), 10, 100 or 1000 ng 3,3',4,4'-tetrachlorobiphenyl (TCB) g(-1) bodyweight, a contaminant found in most arctic fish. After 30 and 90 days of exposure, TCB concentrations in tissues, hepatic phase I activity (as ethoxyresorufin-O-deethylase (EROD)), plasma and tissue vitamin A and E concentrations, plasma thyroid hormone levels and thyroid glandular structure were examined. Total plasma osmolality, as an indicator of overall fish health was also monitored. TCB recovery in tissues was low and extremely variable, making comparisons between intended dose groups inappropriate. Therefore, correlation analysis between actual recovered TCB concentrations and biochemical responses was employed. Hepatic EROD activity correlated strongly with liver TCB concentrations. Liver concentrations of vitamin A were altered as a function of TCB concentrations and EROD activity, but plasma vitamin A status was not affected. Vitamin E was depleted by TCB accumulation in blood and EROD induction in liver of males only at 90 days postexposure. Thyroid hormones status and glandular structure were not affected by the short duration TCB exposures used in this experiment. TCB concentrations were correlated with an elevation in plasma osmolality. Results from this experiment indicate that the vitamin status and osmoregulation of arctic grayling exposed to TCB can be compromised. Further studies of field populations exposed to this type of contaminant are warranted.
authors.affiliation: Department of Fisheries and Oceans, Freshwater Institute, Winnipeg, Manitoba, Canada.
authors.forename: V P
authors.initials: VP
authors.lastname: Palace
authors.forename: S M
authors.initials: SM
authors.lastname: Allen-Gil
authors.forename: S B
authors.initials: SB
authors.lastname: Brown
authors.forename: R E
authors.initials: RE
authors.lastname: Evans
authors.forename: D A
authors.initials: DA
authors.lastname: Metner
authors.forename: D H
authors.initials: DH
authors.lastname: Landers
authors.forename: L R
authors.initials: LR
authors.lastname: Curtis
authors.forename: J F
authors.initials: JF
authors.lastname: Klaverkamp
authors.forename: C L
authors.initials: CL
authors.lastname: Baron
authors.forename: W L
authors.initials: WL
authors.lastname: Lockhart
mesh_terms: D000284:Administration, Oral; D000818:Animals; D019363:Cytochrome P-450 CYP1A1 / Q000378:metabolism*; D004305:Dose-Response Relationship, Drug; D004790:Enzyme Induction; D011078:Polychlorinated Biphenyls / Q000009:adverse effects*; D012487:Salmonidae / Q000502:physiology*; D013963:Thyroid Hormones / Q000032:analysis; D014801:Vitamin A / Q000032:analysis / Q000378:metabolism; D014810:Vitamin E / Q000032:analysis / Q000378:metabolism
chemical_list: D013963:Thyroid Hormones; D014801:Vitamin A; D014810:Vitamin E; D011078:Polychlorinated Biphenyls; D019363:Cytochrome P-450 CYP1A1; C028451:3,4,3',4'-tetrachlorobiphenyl