| In this thesis I examined the acute and sub chronic effects of complete oil sands process affected water (OSPW) and its toxic component, naphthenic acids (NAs). I exposed goldfish for one (acute), or 12 (sub chronic) weeks and examined immune gene expression, macrophage function, the ability of exposed fish to control the infection with Trypanosoma carassii, and endocrine disruption. Acute exposure to 20 mg/L commercial naphthenic acids (C-NAs) or OSPW, induced up-regulation of the expression of immune genes (IFNgamma, IL1-beta1, TNFalpha-2). This up-regulation in gene expression was related to observed increase in macrophage functions in fish exposed to C-NAs, but not in fish exposed to 25% OSPW (NAs content = 10 mg/L). Interestingly, acute exposure of fish to C-NAs or OSPW induced increased resistance to T. carassii. After sub chronic exposures of goldfish to C-NAs or OSPW, a significant decrease in the expression of majority of immune genes was observed, suggesting that the fish were immunosuppressed. This was confirmed by decreased ability of primary macrophages from exposed fish to generate antimicrobial responses. Furthermore, sub chronic exposure of fish to C-NAs caused increased susceptibility to T. carassii, and eventual parasite-induced host mortality. Acute exposure to fresh OSPW induced up-regulation in genes encoding endocrine receptors and higher vitellogenin levels in male fish; while exposure to aged or ozonated OSPW led to a sub chronic alteration in endocrine gene profiles, suggesting a possible long-term endocrine disruption following exposure to ozonated OSPW. Treatment with ozone ameliorated the immunotoxic effects of OSPW, because immune gene expression, macrophage functions and control of T. carassii infecton were similar between ozonated OSPW-exposed and non-exposed goldfish. The results in this thesis represent the first report of immunotoxicity caused by C-NAs or OSPW exposure in aquatic vertebrates. |
