AI Article Synopsis

  • * The study exposed diatoms to a mixture of polycyclic aromatic hydrocarbons (PAHs) from contaminated Mediterranean sediments and compared the results with exposure to individual PAHs, revealing gene regulation linked to stress response, silica uptake, and metabolism.
  • * Findings indicate that while exposure to PAH mixtures and single compounds similarly affects gene expression, some gene responses differ, suggesting that certain genes related to silica uptake could serve as biomarkers for PAH exposure.

Article Abstract

Marine diatoms have a key role in the global carbon fixation and therefore in the ecosystem. We used Thalassiosira pseudonana as a model organism to assess the effects of exposure to environmental pollutants at the gene expression level. Diatoms were exposed to polycyclic aromatic hydrocarbons mixture (PAH) from surface sediments collected at a highly PAH contaminated area of the Mediterranean Sea (Genoa, Italy), due to intense industrial and harbor activities. The gene expression data for exposure to the sediment-derived PAH mixture was compared with gene expression data for in vitro exposure to specific polycyclic aromatic hydrocarbons. The data shows that genes involved in stress response, silica uptake, and metabolism were regulated both upon exposure to the sediment-derived PAH mixture and to the single component. Complementary monitoring of silica in the diatom cultures provide further evidence of a reduced cellular uptake of silica as an end-point for benzo[a]pyrene exposure that could be linked with the reduced gene and protein expression of the silicon transporter protein. However some genes showed differences in regulation indicating that mixtures of structurally related chemical compounds can elicit a slightly different gene expression response compared to that of a single component. The paper provides indications on the specific pathways affected by PAH exposure and shows that selected genes (silicon transporter, and silaffin 3) involved in silica uptake and metabolism could be suitable molecular biomarkers of exposure to PAHs.

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http://dx.doi.org/10.1016/j.aquatox.2010.10.004DOI Listing

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