Reproductive development of yellow perch (Perca flavescens) exposed to oil sands–affected waters

Abstract

In similar experiments conducted in 1996 and 2009, yellow perch (Perca flavescens) were stocked into two experimental systems: a demonstration lake where oil sands fine tailings were capped with natural water and a lake in a watershed containing bitumen-bearing sodic clays. In both experiments, yellow perch were captured in May from a nearby reservoir and released into the experimental ponds. Perch were recaptured in the experimental systems, the source lake, and two reference lakes in late September and lethally sampled to examine reproductive parameters. In the 1996 experiment, gonad size and steroid hormones were not affected in either pond environment. In the 2009 experiment, male perch in the water-capped tailings pond showed a significant reduction in the testicular development and reductions in circulating testosterone and 11-ketotestosterone, while no reductions were seen in the second experimental pond. No changes were observed in ovarian size or circulating steroid levels in female perch. In the pond containing tailings, the release of water from underlying tailings caused approximately a twofold increase in salinity, alkalinity, and naphthenic acids, and a pH increase from 8.4 to 9.4 over the 13-year period of the study. In the pond influenced by unextracted oil sands materials, total dissolved solids, major ions, and pH did not change substantially. However, naphthenic acids in this system dropped more than twofold post-watershed reclamation. Because the selective reproductive effect observed in male perch in the experimental end-pit lake were accompanied by increases in naphthenic acids, alkalinity, and pH, a specific cause cannot be determined. The present study adds to the evidence, suggesting the presence of endocrine-disrupting substances in oil sands.

Toxicity of naphthenic acid fraction components extracted from fresh and aged oil sands process-affected waters, and commercial naphthenic acid mixtures, to fathead minnow (Pimephales promelas) embryos

“…Similarly, both male and female fathead minnow exposed for seven days to fresh OSPW showed altered transcription of estrogen-responsive genes in brain, liver and gonad tissue (He et al, 2012b). Aromatic NAFCs, and not alicyclic NAFCs, may be responsible for these changes , although OSPW alkalinity and pH may also play a role (Van den Heuvel et al, 2012). However, responses extend beyond endocrine disruption.…”

Population impacts in white sucker (Catostomus commersonii) exposed to oil sands–derived contaminants in the Athabasca River

“…Several studies have investigated the effects of oil sands process-affected water exposure on fish physiology [14,15]. Several studies have investigated the effects of oil sands process-affected water exposure on fish physiology [14,15].…”

Disruption of endocrine function in H295R cell in vitro and in zebrafish in vivo by naphthenic acids

“…This result is consistent with the in vitro assay in the current study that CYP19a gene expression was significantly induced in H295R cells in the exposure groups. Combining in vitro and in vivo assays about steroidogenic disruption of NAs, it can be concluded that NAs cause endocrine disrupting effects via steroidogenic modulation, which might be the possible reason for lesser concentrations of T in blood plasma in previous OSPW studies [13][14][15]. Transcription of VTG gene has been developed as a biomarker for estrogenic pollution [47][48][49].…”

“…The endocrine disruption of OSPW has been well documented in vitro [17][18][19][20] and in vivo [9,[13][14][15][16]21]; however, the compounds responsible for the activities in OSPW were not assigned. Although, NAs has been considered as the primary toxic compounds in OSPW, few studies have directly performed the endocrine disrupting function of NAs.…”

“…Currently, sub-lethal concentrations of OSPW have also shown to cause disturbances to the endocrine function and reproductive system. Exposure to OSPW decreased concentrations of testosterone (T) and estradiol (E2) in plasma of yellow perch (P. flavescens) [13], goldfish (C. auratus) [14], and impaired the reproductive capacity of fathead minnows (P. promelas) as exemplified by decreased fecundity, altered synthesis of sex steroid hormones, and less pronounced secondary sex characteristics of male and female minnows [15]. Abundances of transcripts of regulatory genes in all tissues of the brain-gonad-liver axis were significantly different in fathead minnows (P. promelas) exposed to OSPW [16].…”