In April 1997 and 1998 investigations of algae, Rotatoria, Cladocera, Copepoda and Hydracarina were conducted. The investigated localities were 8 small water bodies at around 800 m a.s.l., at Mali Krs, in the surrounding of Bor, Serbia (Yugoslavia). The aim was to examine composition of these groups and to give the evaluation of the quality of water. Among algae, according to the number of taxons, the dominant group was Bacillariophyta (45), then Chlorophyta (17), Cyanophyta (3), Euglenophyta (4), Xanthophyta (1) and Pyrrophyta (1). Rotatoria were present with the highest number of taxons among microfauna. In these investigations 48 taxons were present. The highest number of taxons was among Cephalodella, Corurella, and Trichocerca. Among Cladocera 4 taxons were present, and among Copepoda 9 taxons, and all the present species were found in our previous investigations. Hydracarina were present with 3 species, also with high diversity. Around two thirds of all taxons are oligosaprobionts, which indicates to the good quality of the water.

Diazinon is a common organophosphate pesticide widely used to control parasitic infections in agriculture. Excessive use of diazinon can have adverse effects on the environment and aquatic animal health. In the present study, the toxic effects of diazinon on the histology, antioxidant, innate immune and intestinal microbiota community composition of crucian carp (Carassius auratus gibelio) were investigated. The results showed that diazinon at the tested concentration (300 μg/L) induced gill and liver histopathological damages. Hepatic total superoxide dismutase (T-SOD), catalase (CAT), and glutathione S-transferase (GST) activities significantly decreased (P < 0.05) by 32.47%, 65.33% and 37.34%, respectively. However, the liver tissue malondialdehyde (MDA) content significantly (P < 0.05) increased by 138.83%. The 300 μg/L diazinon significantly (P < 0.05) downregulated the gene expression of TLR4, MyD88, NF-kB p100 and IL-8 but had no significant effect TNF-α (P = 0.8239). In addition, the results demonstrated that diazinon exposure could affect the intestinal microbiota composition and diversity. Taken together, the results of this study indicated that diazinon exposure can cause damage to crucian carp, induce histopathological damage in gill and liver tissues, oxidative stress in the liver, and innate immune disorders and alter intestinal microbiota composition and diversity.

2,6-Dimethylphenol (2,6-DMP), an important chemical intermediate and the monomer of plastic polyphenylene oxide, is widely used in chemical and plastics industry. However, the pollution problem of 2,6-DMP residues is becoming increasingly serious, which is harmful to some aquatic animals. Microbial degradation provided an effective approach to eliminate DMPs in nature, which is considered as a prospective way to remediate DMPs-contaminated environments. But the 2,6-DMP-degrading bacteria is not available and the molecular mechanism of 2,6-DMP degradation is unclear as well. Here, a 2,6-DMP-degrading bacterium named B5-4 was isolated and identified as Mycobacterium neoaurum. M. neoaurum B5-4 could utilize 2,6-DMP as the sole carbon source for growth. Furthermore, M. neoaurum B5-4 could degrade 2,6-DMP with concentrations ranging from 1 to 500 mg L⁻¹. Six intermediate metabolites of 2,6-DMP were identified and a metabolic pathway of 2,6-DMP in M. neoaurum B5-4 was proposed, in which 2,6-DMP was initially converted to 2,6-dimethyl-hydroquinone and 2,6-dimethyl-3-hydroxy-hydroquinone by two consecutive hydroxylations at C-4 and γ position; 2,6-dimethyl-3-hydroxy-hydroquinone was then subjected to aromatic ring ortho-cleavage to produce 2,4-dimethyl-3-hydroxymuconic acid, which was further transformed to citraconate, and subsequently into TCA cycle. In addition, toxicity bioassay of 2,6-DMP in water using zebrafish indicates that 2,6-DMP is toxic to zebrafish and M. neoaurum B5-4 could effectively eliminate 2,6-DMP in water to protect zebrafish from 2,6-DMP-induced death. This work provides a potential strain for bioremediation of 2,6-DMP-contaminated environments and lays a foundation for elucidating the molecular mechanism and genetic determinants of 2,6-DMP degradation.

Effective measures for protecting and preserving the marine environment require an understanding of the potential impact of anthropogenic sound on marine life. A crucial component is a proper assessment of the anthropogenic soundscape: which sounds are present where, when and how strong? We provide an extensive case study modelling the spatial, temporal and spectral distribution of sound radiated by several anthropogenic sources (ships, seismic airguns, explosives) and a naturally occurring one (wind) in the Dutch North Sea. We present the results as a series of sound maps covering the whole of the Dutch North Sea, showing the spatial and temporal distribution of the energy from these sources. Averaged over a two year period, shipping is responsible for the largest amount of acoustic energy (∼1800 J), followed by seismic surveys (∼300 J), explosions (∼20 J) and wind (∼20 J) in the frequency band between 100 Hz and 100 kHz. Our study shows that anthropogenic sources are responsible for 100 times more acoustic energy (averaged over 2 years) in the Dutch North Sea than naturally occurring sound from wind. The potential impact of these sounds on aquatic animals depends not only on these temporally averaged and spatially integrated broadband energies, but also on the source-specific spatial, spectral and temporal variation. Shipping is dominant in the southern part and along the coast in the north, throughout the years and across the spectrum. Seismic surveys are relatively local and spatially and temporally dependent on exploration activities in any particular year, and spectrally shifted to low frequencies relative to the other sources. Explosions in the southern part contribute wide-extent high energy bursts across the spectrum. Relating modelled sound fields to the temporal and spatial distribution of animal species may provide a powerful tool for understanding the potential impact of anthropogenic sound on marine life.

Due to their longevity and extensive migration areas, marine turtles are able to accumulate diverse contaminants over many years and as a consequence they represent an interesting bioindicator species for marine ecosystem pollution. Metals provoke toxicological effects in many aquatic animal species, but marine turtles have been under-investigated in this area. Thus, we have determined the presence of certain inorganic elements (As, Cd, Cu, Ni, Pb, Se and Zn) in olive ridley turtles (Lepidochelys olivacea) and related them to metallothionein (MT), superoxide dismutase (SOD), catalase (CAT) and glutathione reductase (GR) transcription and/or enzymatic activities. Gene expression of sod, cat and gr was found to be higher in blood than liver or kidney but most of the significant relationships were found in liver, not only for gene expression but also for enzyme activities. This must be related to the role the liver has as the first filter organ. Several positive relationships of sod, cat and gr gene expression in the different tissues were found in this population, as well as very high Cd concentrations. This could mean that these turtles are adapting to the metals-production of ROS and damage through a high transcription of these antioxidants. Multiple positive relationships with GR seem to be part of its compensatory effect due to the decrease of SOD production against the high and chronic exposure to certain xenobiotics. CAT, on the other hand, seems not to be used much, and glutathione detoxification of H₂O₂ may be more important in this species. Finally, despite the very high Cd concentrations found in this population, no significant relationship was found in any tissue with metallothionein gene expression. These results, along with very high Cd concentrations and a negative relationship with Cu, lead us to consider some kind of disruption in mt gene expression in these turtles.

Microcystin-LR (MC-LR) is the most abundant toxicant among microcystin variants produced by cyanobacteria. MC-induced toxicity is broadly reported to pose a threat to aquatic animals and humans and has been associated with the dysfunction of some organs such as liver and kidney. However, MC-induced neurotoxicity has not been well characterized after long-term exposure. This study was designed to investigate the neurotoxic effects after chronic oral administration of MC-LR. In our trial, C57/BL6 mice received MC-LR at 0, 1, 5, 10, 20 and 40 μg/L in drinking water for twelve months. Our data demonstrated that mitochondrial DNA (mtDNA) damage was evident in the damaged neurons as a result of chronic exposure. Histopathological abnormalities and mtDNA damage were observed in the hippocampus and cerebral cortex. Furthermore, MC-LR exerted distinct effects on these two brain regions. The hippocampus was more susceptible to the treatment of MC-LR compared with the cerebral cortex. However, no strong relationships were observed between the genotoxic effects and exposure doses. In conclusion, this study has provided a mtDNA-related mechanism for underlying chronic neurotoxicity of MC-LR and suggested the presence of differential toxicant effects on the hippocampus and cerebral cortex.

This review evaluates the three dynamic models (biokinetic model: BK, physiologically based pharmacokinetic model: PBPK, and toxicokinetic-toxicodynamic model: TKTD) in our understanding of the key questions in metal ecotoxicology in aquatic systems, i.e., bioaccumulation, transport and toxicity. All the models rely on the first-order kinetics principle of metal uptake and elimination. The BK model basically treats organisms as a single compartment, and is both physiologically and geochemically based. With a good understanding of each kinetic parameter, bioaccumulation of metals in any aquatic organisms can be studied holistically and mechanistically. Modeling efforts are not merely restrained from the prediction of metal accumulation in the tissues, but instead provide the direction of the key processes that need to be addressed. PBPK is more physiologically based since it mainly addresses the transportation, transformation and distribution of metals in the organisms. It can be treated conceptually as a multi-compartmental kinetic model, whereas the physiology is driving the development of any good PBPK model which is no generic for aquatic animals and contaminants. There are now increasingly applications of the PBPK modeling specifically in metal studies, which reveal many important processes that are impossible to be teased out by direct experimental measurements without adequate modeling. TKTD models further focus on metal toxicity in addition to metal bioaccumulation. The TK part links exposure and bioaccumulation, while the TD part links bioaccumulation and toxic effects. The separation of TK and TD makes it possible to model processes, e.g., toxicity modification by environmental factors, interaction between different metals, at both the toxicokinetic and toxicodynamic levels. TKTD models provide a framework for making full use of metal toxicity data, and thus provide more information for environmental risk assessments. Overall, the three models reviewed here will continue to provide guiding principles in our further studies of metal bioaccumulation and toxicity in aquatic organisms.