Metals(loids) targeting fish eyes and brain in a contaminated estuary - Uncovering neurosensory (un)susceptibility through bioaccumulation, antioxidant and morphometric profiles

Abstract

This study examined the susceptibility of fish (Liza aurata) eyes and brain to metals(loids) contamination under realistic exposure conditions. A multidimensional approach was applied to fish caught at a chronically contaminated site (BAR) and at a reference site of the Tagus estuary (Portugal), which comprised metals(loids) accumulation in eyes and brain together with a battery of enzymatic and non-enzymatic antioxidants, as well as brain morphometry (i.e. cell density). Trace element levels in the blood, gills, liver and kidney allowed interpretations on their preferential pathway(s) to the eyes and brain. Metals(loids) accumulation pointed out the elevated vulnerability of the fish eyes at BAR, probably related with the direct waterborne uptake. Pb uptake in L. aurata eyes could be associated both with water and indirect pathways. At the most contaminated site, metals(loids) were on the basis of pro-oxidant conditions in the ocular tissues, while no indication of toxicity was recorded in the brain. Overall, the results disclosed a differential bioaccumulation among fish organs, suggesting that, in the L. aurata population studied, metal organotropism underlie the lower susceptibility of the brain comparing to the eyes. However, mechanisms remain little understood and further work is needed.

A multidimensional concept for mercury neuronal and sensory toxicity in fish - From toxicokinetics and biochemistry to morphometry and behavior

“…At Aveiro lagoon, that is almost exclusively contaminated by Hg at a confined area (Laranjo), Hg triggered a deficit in cell density of Liza aurata hypothalamus during the winter, while in the summer it promoted larger volumes of the optic tectum and cerebellum [250]. Differently, L. aurata caught at an impacted area of the Tagus estuary (Portugal), including by Hg, did not displayed any brain morphometric changes when assessed by cell density of the lateral pallium, hypothalamus, optic tectum and cerebellum [249]. The discrepancy between field and laboratory studies for the effects of Hg in the fish brain can be related with a number of factors, ranging from differences between fish species and its origin (wild vs. fish farm) to differences in exposure levels.…”

“…It is worth revisiting that the diet is the most relevant route of MeHg exposure in fish in the natural environment, while water has a higher preponderance for fish exposure to iHg, suggesting that conclusions provided by studies that did not used that binomial combination of exposure route and Hg form should be analyzed critically. There are also two studies that consisted in the brain morphometric analysis of wild fish from Hg contaminated areas located in Portugal [249,250], but effects of Hg in the brain were not very expressive, pointing out dissimilarity of field and laboratory findings that need to be clarified. Research on the morpho-structural effects of Hg on fish sensory organs is still missing, even if the first publication is from 1975 and reported effects on the olfactory organs and lateral line [242].…”

“…Previous findings were made in juvenile and adult specimens of seawater fish, namely: S. salar [36]; D. sargus [23,24]; S. pavo [248] and L. aurata [249,250]. Besides that, the ultra-structural effects of waterborne MeHg on embryonic zebrafish neurons were also investigated using transmission electron microscopy [247].…”

Teratogenic and Neurotoxic Effects of n‐Butanol on Zebrafish Development

“…With this study, adverse effects of n‐butanol on eye development were determined, and in high doses of n‐butanol (500, 750 and 1,000 mg/L) the formation of vacuoles in the brain (spongi degeneration) with eye development of the embryo and larvae reveals an important effect. Both organs are well protected with histophysiological barriers, namely the blood‐retinal barrier and the blood‐brain barrier (Pereira et al 2018). However, low molecular weight lipophilic compounds (such as alcohol) can passively spread to the brain and retina via a cellular route (Hitchcock and Pennington 2006).…”