Phosphorus application enhances alkane hydroxylase gene abundance in the rhizosphere of wild plants grown in petroleum-hydrocarbon-contaminated soil.

This study assessed the ability of phosphorus (P) fertilizer to remediate the rhizosphere of three wild plant species (Banksia seminuda, a tree; Chloris truncata, a grass; and Hakea prostrata, a shrub) growing in a soil contaminated with total (aliphatic) petroleum hydrocarbon (TPH). Plant growth, photosynthesis (via chlorophyll fluorescence), soil microbial activity, alkane hydroxylase AlkB (aliphatic hydrocarbon-degrading) gene abundance, and TPH removal were evaluated 120 days after planting. Overall, although TPH served as an additional carbon source for soil microorganisms, the presence of TPH in soil resulted in decreased plant growth and photosynthesis. However, growth, photosynthesis, microbial activities, and AlkB gene abundance were enhanced by the application of P fertilizer, thereby increasing TPH removal rates, although the extent and optimum P dosage varied among the plant species. The highest TPH removal (64.66%) was observed in soil planted with the Poaceae species, C. truncata, and amended with 100 mg P kg-1 soil, while H. prostrata showed higher TPH removal compared to the plant belonging to the same Proteaceae family, B. seminuda. The presence of plants resulted in higher AlkB gene abundance and TPH removal relative to the unplanted control. The removal of TPH was associated directly with AlkB gene abundance (R2 > 0.9, p < 0.001), which was affected by plant identity and P levels. The results indicated that an integrated approach involving wild plant species and optimum P amendment, which was determined through experimentation using different plant species, was an efficient way to remediate soil contaminated with TPH.

Offspring of metal contaminated saltmarsh (Juncus acutus) exhibit tolerance to the essential metal Zn but not the nonessential metal Pb.

Halophytes residing in metal-contaminated saltmarsh habitats may employ strategies to enhance fitness of the next generation. We aimed to test the hypothesis that Juncus acutus individuals inhabiting metal-contaminated locations would experience elevated tolerance of offspring to metals compared to plants residing in locations with no metal contamination history. J. acutus seeds (F1 generation) were collected from F0 parent plants residing at eight locations of a contemporary sediment metal gradient (contaminated to uncontaminated) across the coast of NSW, Australia (Hunter river, Lake Macquarie and Georges River). Seeds were exposed in the laboratory to incremental Zn (0.0-1.6 mM) and Pb (0.0-0.50 mM) for nine (9) days, and % germination, germination rate, root elongation and vigour index were assessed for the determination of tolerance. Greater root accumulation (BCF = 1.01) of Zn and subsequent translocation to aerial parts (culm BCF = 0.58 and capsule BCF = 0.85) were exhibited in parents plants, whereas Pb was excluded from roots (BCF = 0.60) and very little translocation to aerial portions of the plant was observed (culm BCF = 0.02 and capsule BCF = 0.05). F1 offspring exhibited tolerance to Zn with EC50 (% germination) significantly correlated with their parents' culm (R2 = 0.93, p = 0.00) and capsule (R2 = 0.57; p = 0.03) Zn. No correlations were observed between offspring Pb tolerance and Pb in parents' plant tissues. Enhanced tolerance to the essential metal Zn may be because Zn is very mobile in the parent plant and seeds experience greater Zn load as a significant portion of sediment Zn reaches capsules (85%). Thus, Zn tolerance in J. acutus seeds is likely attributable to acclimation via maternal transfer of Zn; however, further manipulative experiments are required to disentangle potential acclimation, adaptation or epigenetic effects in explaining the tolerance observed.

Estrogenic mixtures induce alterations in lipidomic profiles in the gonads of female oysters.

This study aimed to reveal possible alterations to lipidomic profiles in Sydney rock oysters, Saccostrea glomerata, exposed to estrogenic mixtures (i.e., estrone, E1; 17ß-estradiol, E2; estriol, E3; 17α-ethinylestradiol, EE2; bisphenol A, BPA; 4-t-octylphenol, 4-t-OP; and 4-nonylphenol, 4-NP) at "low" and "high" concentrations, typical of those detected in Australian and global receiving waters. A seven-day acute exposure window exhibited significantly lower abundances of many non-polar metabolites in digestive gland, gills, and gonads. Overall, there was a strong effect of the carrier solvent ethanol (despite a low exposure of 0.0002%), with all solvent containing treatments exhibiting lower abundances of lipidic metabolites, especially in the gill and digestive gland. No significant changes of the lipidome were exhibited in the male gonad by estrogenic exposure. However, in the female gonad, significant reductions of phospholipids and phosphatidylcholine were associated with exposure to high estrogenic mixtures. We hypothesise that the decreases in these phospholipids in the female gonad may be attributable to 1) lower algal consumption and thus lower uptake of lipidic building blocks; 2) a reduction of available substrates for phospholipid and phosphatidylcholine synthesis; and/or 3) induction of reactive oxygen species via estrogen metabolism, which may cause lipid peroxidation and lower abundance of phospholipids.

Parental exposure to the synthetic estrogen 17α-ethinylestradiol (EE2) affects offspring development in the Sydney rock oyster, Saccostrea glomerata.

Very little is currently known regarding the effects of estrogenic endocrine disrupting chemicals on embryonic and larval development in molluscs, nor the potential effects of parental (F0) exposure on resultant F1 offspring. In this study, we assessed the embryotoxic impacts of exposure to environmentally relevant concentrations of the synthetic estrogen, 17α-ethinylestradiol (EE2), to male and female parents (50 ng/L) and their offspring (5 and 50 ng/L) in the native Australian Sydney rock oyster, Saccostrea glomerata. There were no detectable effects of parental exposure on fertilisation success, proportions of early larval (F1) morphs and unfertilised eggs. Offspring impacts were evidenced in terms of developmental delays, with decreased percentages of D-veligers retained by 45 µm mesh, along with a reduction of swimming capabilities of larvae at 2 days post-fertilisation (dpf) when both parents had been exposed to 50 ng/L EE2. Although no significant parental effects were found on the survival of F1 larvae at 9 dpf, retardation of shell growth was observed on F1 larvae in treatments where both parents had been exposed to 50 ng/L EE2. Subsequent larval exposure from 2 to 9 dpf caused declines in survival and reduction of shell length in F1 larvae at both 5 and 50 ng/L EE2 across all parental exposure treatments. Collectively, parental EE2 imparts effects on offspring in terms of retardation of larval development, and subsequent offspring exposure to EE2 further exacerbates impacts to development. Future research should aim to understand the potential mechanisms of EE2 induced toxicity and its transmission resulting in altered phenotypes of the F1 generation.