Publications by authors named "Marianne Woods"

The contamination of major continental river systems by endocrine-active chemicals (EACs) derived from the discharge of wastewater treatment plant (WWTP) effluents can affect human and ecosystem health. As part of a long-term effort to develop a native fish model organism for assessment of endocrine disruption in Australia's largest watershed, the Murray-Darling River Basin, the present study evaluated endocrine disruption in adult males of the native Australian Murray rainbowfish (Melanotaenia fluviatilis) exposed to effluent from an activated sludge WWTP and water from the Murray River during a 28-d, continuous-flow, on-site experiment. Analysis of the WWTP effluent and river water detected estrone and 17β-estradiol at concentrations up to approximately 25 ng L(-1) .

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Hepatic vitellogenin (VTG) mRNA and plasma protein assays were developed for the Murray rainbowfish (Melanotaenia fluviatilis), a native freshwater fish species in Australia. Adult male Murray rainbowfish were exposed to 17β-estradiol (E2) or 17α-ethynylestradiol (EE2) at 0, 1, 5, 10, 50, or 100 ng/L in a semistatic system for 7 d. Vitellogenin mRNA was quantified by quantitative polymerase chain reaction, and VTG protein was semiquantified in plasma using an enzyme-linked immunosorbent assay.

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Estrogens are steroidal hormones that control many physiological processes in both female and male vertebrates. Like other vertebrates, fish have two distinct estrogen receptors (Esr) subtypes, Esr1 and Esr2a that have been isolated in a number of species, as well as a third subtype, Esr2b. The mRNA encoding the Esr1 was isolated from the female liver of an Australian freshwater fish, the Murray rainbowfish, Melanotaenia fluviatilis.

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The localisation of estrogen receptors (ERalpha and ERbeta) and vitellogenin (VTG) transcripts were examined in the liver and testis in male rainbowfish exposed to 17beta-estradiol (E2; 0, 50 and 500 ng/L) via the water for up to 7 days. The ER transcripts were localised within the perinuclear region of the hepatocytes and were up-regulated with E2 exposure. A parallel induction of liver VTG transcripts and protein was observed within 24h, followed by a time-dependent increase in VTG protein.

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