Fish eyes and brain are highly susceptible to environmental Hg exposure but this issue is still scarcely investigated, mainly regarding methylmercury (MeHg) accumulation. Yet, Hg levels in fish lens have not been previously examined under field conditions. Total Hg (tHg), MeHg and inorganic Hg (iHg) levels were assessed in the brain, eye wall and lens of the golden grey mullet (Liza aurata) from an Hg contaminated area, both in winter and summer, together with water and sediment levels. Sampling was performed at Aveiro lagoon (Portugal) where a confined area (LAR) is severely contaminated by Hg. Fish brain, eye wall and lens accumulated higher levels of tHg, MeHg and iHg at LAR than the reference site, reflecting faithfully environmental spatial differences. The brain and eye wall responded also to the winter-summer changes found in water and sediment, accumulating higher levels of MeHg (and tHg) in winter. Contrarily, lens was unable to reflect seasonal changes, probably due to its composition and structural stability over time. The three neurosensory structures accumulated preferentially MeHg than iHg (MeHg was higher than 77% of tHg). Lens exhibited a higher retention capacity of MeHg (mean around 1 μg g(-1) at LAR), accumulating higher levels than the other two tissues. Interestingly, MeHg and iHg levels were significantly correlated for the brain and eye wall but poorly associated within the two analysed eye components. The high levels of MeHg found in the brain, eye wall and lens could compromise their functions and this needs further research.

The current study contributes to fill the knowledge gap on the neurotoxicity of inorganic mercury (iHg) in fish through the implementation of a combined evaluation of brain morphometric alterations (volume and total number of neurons plus glial cells in specific regions of the brain) and swimming behavior (endpoints related with the motor activity and mood/anxiety-like status). White seabream (Diplodus sargus) was exposed to realistic levels of iHg in water (2μgL(-1)) during 7 (E7) and 14 days (E14). After that, fish were allowed to recover for 28 days (PE28) in order to evaluate brain regeneration and reversibility of behavioral syndromes. A significant reduction in the number of cells in hypothalamus, optic tectum and cerebellum was found at E7, accompanied by relevant changes on swimming behavior. Moreover, the decrease in the number of neurons and glia in the molecular layer of the cerebellum was followed by a contraction of its volume. This is the first time that a deficit on the number of cells is reported in fish brain after iHg exposure. Interestingly, a recovery of hypothalamus and cerebellum occurred at E14, as evidenced by the identical number of cells found in exposed and control fish, and volume of cerebellum, which might be associated with an adaptive phenomenon. After 28 days post-exposure, the optic tectum continued to show a decrease in the number of cells, pointing out a higher vulnerability of this region. These morphometric alterations coincided with numerous changes on swimming behavior, related both with fish motor function and mood/anxiety-like status. Overall, current data pointed out the iHg potential to induce brain morphometric alterations, emphasizing a long-lasting neurobehavioral hazard.

Clarification of the mechanisms of mercury (Hg) toxicity in fish remains challenging. An innovative approach to this clarification is the combined assessment of metabolomic shifts, alterations in the antioxidant system and the risk of oxidative damage, and Hg bioaccumulation. This strategy was applied to the livers of golden grey mullet (Liza aurata) inhabiting an Hg-contaminated system in Aveiro Lagoon, Portugal. Marked changes in both the metabolic profile and the response to antioxidants were observed in fish exposed to Hg in the environment, indicating their compromised state of health. The metabolomics analysis showed a clear differentiation between the contaminated and uncontaminated areas, revealing that Hg has multiple levels of impact, including membrane stabilization/degradation/repair processes, osmoregulation, energy metabolism, gene expression and antioxidant protection. Research on oxidative stress biomarkers showed that Hg triggered adaptive responses in the antioxidant system as seen by an increase in the activities of glutathione-S-transferase and catalase, as well as the total glutathione content, which compensated for a decrease in glutathione peroxidase activity. The integration of metabolomics and oxidative stress endpoints allowed the identification of reduced glutathione as a first line of defence against Hg and evidenced oxidative insults in cell membranes, recognized through the increase in phosphatidylcholine degradation products (phosphocholine and glycerophosphocholine). Despite these effects, the induction of lipid peroxidation was efficiently prevented. The triad approach used here was demonstrated to be sensitive and effective towards a mechanistically based assessment of Hg hepatotoxicity in fish.

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