Acute Effects of Mercuric Chloride on the Olfactory Epithelium of Trichomycterus brasiliensis

doi:10.1006/eesa.1995.1049

Ecotoxicology and Environmental Safety

Volume 31, Issue 2, July 1995, Pages 104-109

https://doi.org/10.1006/eesa.1995.1049 Get rights and content

Abstract

The olfactory organ in fish has a distinct localization, a major biological significance, and an important role in fish behavior. One group of Trichomycterus brasiliensis was exposed to two different concentrations of mercuric chloride (0.05 and 0.1 mg HgCl₂ liter⁻¹). The surface of the olfactory epithelium was investigated with scanning electron microscopy. Forty individuals were used in this study. The olfactory epithelia were collected after 4, 12, 24, 48, and 96 hr from contaminated and control aquaria. In the experiment with 0.1 mg HgCl₂ liter⁻¹ all individuals died within 24 hr with significant damage to the olfactory epithelium. Type 1 ciliated cells were the most evidently altered. With 0.05 mg HgCl₂ liter⁻¹ the initial alterations were considerable, but after 96 hr the epithelial surface recovered its initial appearance compared with the control individuals. This recovery is due to the resistance of this species and to the decrease in the Hg²⁺ concentration in water. Therefore, the alterations observed in this study reveal that inorganic mercury affects the olfactory organs structurally, with evident interference with normal behavior.

References (0)

Cited by (25)

Neurobehavioral and immune-toxic impairments induced by organic methyl mercury dietary exposure in Nile tilapia Oreochromis niloticus
2021, Aquatic Toxicology
Citation Excerpt :
Until recently, limited information was available regarding MeHg toxicity in fish and there are no studies concerning sub-chronic impacts of different MeHg dietary doses on freshwater Nile tilapia. In fish, utmost studies on Hg prompted brain regional pathology and behavior modifications are limited to water-borne exposure, reporting olfactory organs structural damage, and sensory behavior disruption (Baatrup et al., 1990; 1991;Ribeiro et al., 1995). Embryonic exposure to different concentrations of MeHg in aquaria water induced changes in the hatchlings behavior of feeding and predator avoidance (Weis and Weis, 1995; Fjeld et al., 1998), which may be owing to the reduction of locomotor ability (Zhou and Weis, 1998).
Although substantial knowledge of mercury toxicity in fish has been assembled; until now, studies investigating the toxic impacts in Nile tilapia (Oreochromis niloticus) following dietary exposure to organic methyl mercury (MeHg) are less prolific. Accordingly, the current study aimed to evaluate the impacts of MeHg on neurobehavioral and immune integrity in Nile tilapia after dietary exposure. Two hundred and twenty-five juvenile Nile tilapia (19.99 ± 0.33 g) were allocated into five groups in triplicates (15 fish/replicate). G1, G2, G3, G4, and G5. O. niloticus were fed corresponding basal diets containing 0, 0.5, 1, 1.5, and 2 mg/kg diet MeHg chloride (MeHgCl) daily for 30 days, zero value represented the control G1 group. The results showed that MeHg induced significant alterations in O. niloticus behavior, the swimming behavior was significantly decreased, while scratching, biting, and fin tugging behaviors were significantly augmented. Moreover; chasing, mouth pushing, and butting behaviors were significantly increased in all the exposed groups. MeHg significantly decreased brain acetylcholine esterase (AChE) and serum immunoglobulin M (IgM) levels in all the exposed groups. Meanwhile, serum levels of lysozyme (LYZ), nitric oxide (NO), superoxide dismutase (SOD) malondialdehyde (MDA), protein carbonyl (PCO), and 8 hydroxy 2 deoxyguanosine (8OH2dG) were significantly elevated in all the exposed groups except for serum reduced glutathione (GSH) content was significantly decreased implying oxidative stress (OS), lipid peroxidation (LPO), protein, DNA damage and impaired immune response of the exposed tilapia. MeHg significantly altered transcriptional expression of immune-related genes including (TNF-α, IL-1β, and IL-8, and IL-10) in all the exposed groups. From the obtained outcomes, the present research is the premier to investigate that dietary MeHg exposure in O. niloticus significantly induced neurobehavioral and immune defense impairments in a dose-related manner. This study exhibits that dietary MeHg may pose a potential threat to the O. niloticus populations.
A multidimensional concept for mercury neuronal and sensory toxicity in fish - From toxicokinetics and biochemistry to morphometry and behavior
2019, Biochimica et Biophysica Acta - General Subjects
Citation Excerpt :
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]. More recently, studies have been focused on the effects of Hg forms on the taste buds [251], olfactory epithelium [252,253] and eyes [162,230], while no information is available on fish ear. Berntssen and colleagues [36] performed a histopathological analysis of the Atlantic salmon (Salmo salar) brain after long-term dietary exposure (120 days) to MeHg (4.3 and 8.6 μg g-1 dw) and HgCl2 (10 and 100 μg g-1 dw, corresponding to 7.4 and 74 μg g-1 of Hg2+).
Neuronal and sensory toxicity of mercury (Hg) compounds has been largely investigated in humans/mammals with a focus on public health, while research in fish is less prolific and dispersed by different species. Well-established premises for mammals have been governing fish research, but some contradictory findings suggest that knowledge translation between these animal groups needs prudence [e.g. the relative higher neurotoxicity of methylmercury (MeHg) vs. inorganic Hg (iHg)]. Biochemical/physiological differences between the groups (e.g. higher brain regeneration in fish) may determine distinct patterns. This review undertakes the challenge of identifying sensitive cellular targets, Hg-driven biochemical/physiological vulnerabilities in fish, while discriminating specificities for Hg forms.
A functional neuroanatomical perspective was conceived, comprising: (i) Hg occurrence in the aquatic environment; (ii) toxicokinetics on central nervous system (CNS)/sensory organs; (iii) effects on neurotransmission; (iv) biochemical/physiological effects on CNS/sensory organs; (v) morpho-structural changes on CNS/sensory organs; (vi) behavioral effects. The literature was also analyzed to generate a multidimensional conceptualization translated into a Rubik’s Cube where key factors/processes were proposed.
Hg neurosensory toxicity was unequivocally demonstrated. Some correspondence with toxicity mechanisms described for mammals (mainly at biochemical level) was identified. Although the research has been dispersed by numerous fish species, 29 key factors/processes were pinpointed.
Future trends were identified and translated into 25 factors/processes to be addressed. Unveiling the neurosensory toxicity of Hg in fish has a major motivation of protecting ichtyopopulations and ecosystems, but can also provide fundamental knowledge to the field of human neurodevelopment.
Brain as a critical target of mercury in environmentally exposed fish (Dicentrarchus labrax)-Bioaccumulation and oxidative stress profiles
2011, Aquatic Toxicology
Citation Excerpt :
Notwithstanding that mercury neurotoxicity has been well reported in both humans and mammalian models (Stohs and Bagchi, 1995; Clarkson et al., 2003; Aschner et al., 2007; Stringari et al., 2008), the knowledge regarding mercury threat to fish brain is still limited to a small number of published works. The available fish studies report neurodegenerative damage, including disturbances on sensory capacities (Baatrup et al., 1990; Oliveira Ribeiro et al., 1995), lipid peroxidative injury and necrotic lesions in brain, as well as behaviourial changes (Berntssen et al., 2003). In addition, Mieiro et al. (2009) found that fish brain can have an important role in biomagnification processes, highlighting its importance in environmental risk assessment.
Although mercury is recognized as a potent neurotoxicant, information regarding its threat to fish brain and underlying mechanisms is still scarce. In accordance, the objective of this work was to assess vulnerability of fish to mercury neurotoxicity by evaluating brain pro-oxidant status in wild European sea bass (Dicentrarchus labrax) captured in an estuarine area affected by chlor-alkali industry discharges (Laranjo Basin, Ria de Aveiro, Portugal). To achieve this goal, brain antioxidant responses such as catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST) activities and total glutathione (GSHt) content were measured. Additionally, damage was determined as lipid peroxidation. To ascertain the influence of seasonal variables on both mercury accumulation and oxidative stress profiles, surveys were conducted in contrasting conditions—warm and cold periods. In the warm period, brain of fish from mercury contaminated sites exhibited ambivalent antioxidant responses, viz. higher GR activity and lower CAT activity regarded, respectively, as possible signs of protective adaptation and increased susceptibility to oxidative stress challenge. Though the risk of an overwhelming ROS production cannot be excluded, brain appeared to possess compensatory mechanisms and was able to avoid lipid peroxidative damage. The warm period was the most critical for the appearance of oxidative damage as no inter-site alterations on oxidative stress endpoints were detected in the cold period. Since seasonal differences were found in oxidative stress responses and not in mercury bioaccumulation, environmental factors affected the former more than the latter. This work increases the knowledge on mercury neurotoxicity in feral fish, highlighting that the definition of critical tissue concentrations depends on environmental variables.
Mercury contamination in spotted seatrout, Cynoscion nebulosus: An assessment of liver, kidney, blood, and nervous system health
2010, Science of the Total Environment
Citation Excerpt :
The exposure levels used in these studies have frequently been at levels greater than those that occur now in natural systems. This limitation has been recognized, and in recent years several investigators have begun to characterize the physiological impacts of relevant exposures of fish to methylmercury and have found reproductive impairment (Matta et al., 2001; Hammerschmidt et al., 2002; Drevnick and Sandheinrich, 2003), oxidative stress (Gonzalez et al., 2005), morphological damage to gills and the olfactory epithelium (Jagoe et al., 1996; Oliveira Ribeiro et al., 1996, 2000), and histopathological effects on liver, kidney, spleen, and other tissues (Filenko et al., 1989; Skak and Baatrup, 1993; Handy and Penrice, 1993; Banerjee and Bhattacharya, 1994; Oliveira Ribeiro et al., 1995, 1996, 2002; Mela et al., 2007). Mercury-associated changes in neurochemical biomarkers have also been documented in other organisms (Basu et al., 2007; Scheuhammer et al., 2008) and there is a need to examine these specific biomarkers in fish.
Marine fishes in South Florida (Florida Keys–Florida Bay–Everglades region) accumulate higher concentrations of mercury (Hg) in their tissues than similar fishes from other areas of the southeastern U.S., though it is not known whether these elevated levels affect fish health. In this study, we used quantifiable pathological and biochemical indicators to explore Hg-associated differences in marine fish from South Florida, where Hg contamination is high, and from Indian River Lagoon, Florida, which served as a reference area. Hg concentrations in all tissues of mature spotted seatrout (Cynoscion nebulosus) from South Florida were significantly higher than those from Indian River Lagoon and were within the threshold range of those in studies where effects of Hg exposure have been observed. The distribution of Hg among tissues followed the same trend in both areas, with the greatest concentration in kidney tissue, followed by liver, muscle, brain, gonad, and red blood cells. Blood-plasma biochemistry showed that concentrations of iron, inorganic phosphate, lactate dehydrogenase, and aspartate aminotransferase were significantly less in South Florida. Also, fructosamine and alkaline phosphatase were significantly less in South Florida. Liver histology revealed that pyknosis/necrosis, interstitial inflammation, and bile duct hyperplasia were found only in seatrout from South Florida, and steatosis/glycogen was more frequently found in Indian River Lagoon specimens. In renal tissue, interstitial inflammation, glomerular dilatation and thickening, and tubular degeneration and necrosis were more frequently found in South Florida specimens. Changes in the liver cytoskeleton and morphology may explain some of the differences in blood parameters between study areas. Neurochemical analyses showed that brain N-methyl-d-aspartic acid (NMDA) receptors (but not those of muscarinic cholinergic receptors, monoamine oxidase, or acetylcholinesterase) were significantly less in fish from South Florida than from Indian River Lagoon. These findings provide compelling evidence that elevated Hg could cause quantifiable pathological and biochemical changes that might influence the health of spotted seatrout and could also affect other marine fish species.
Developmental selenomethionine and methylmercury exposures affect zebrafish learning
2010, Neurotoxicology and Teratology
Citation Excerpt :
Since deficits were seen in the behavioral task and brain morphology in all regions of the telencephalon was altered (Fig. 6A–C; Table 6A–C), perhaps abnormal growth within the telencephalon, especially the dorsal and lateral regions, contributed to the delay in spatial task learning. These conclusions do not rule out other mechanisms of the central or peripheral nervous systems, e.g., alterations in sensory neuron function [2,15,22,46,60,71], that could contribute to decreases in sensitivity to the mechanical, odor, or visual stimuli required for learning the spatial alternation task and/or information processing that would result in the appearance of a learning deficit. Reduced sensory neuron activation may lessen the fish's ability to extract information about its environment and facilitate an appropriate decision-making process.
Methylmercury (MeHg) is a ubiquitous environmental pollutant and has been shown to affect learning in vertebrates following relatively low exposures. Zebrafish were used to model long-term learning deficits after developmental MeHg exposure. Selenomethionine (SeMet) co-exposure was used to evaluate its role in neuroprotection. Embryos were exposed from 2 to 24 h post fertilization to (1) MeHg without SeMet, (2) SeMet without MeHg and (3) in combination of MeHg and SeMet. In case (1), the levels of MeHg were 0.00, 0.01, 0.03, 0.06, 0.10, and 0.30 μM. In case (2), the levels of SeMet were 0.00. 0.03, 0.06, 0.10, and 0.30 μM. In case (3), co-exposure levels of (MeHg, SeMet) were (0.03, 0.03), (0.03, 0.06), (0.03, 0.10), (0.03, 0.30), (0.10, 0.03), (0.10, 0.06), (0.10, 0.10), and (0.10, 0.30) μM. Learning functions were tested in individual adults, 4 months after developmental exposure using a spatial alternation paradigm with food delivery on alternating sides of the aquarium. Low levels of MeHg (< 0.1 µM) exposure delayed learning in treated fish; fish exposed to higher MeHg levels were unable to learn the task; SeMet co-exposure did not prevent this deficit. These data are consistent with findings in laboratory rodents. The dorsal and lateral telencephalon are the primary brain regions in fish involved in spatial learning and memory. Adult telencephalon cell body density decreased significantly at all MeHg exposures > 0.01 μM MeHg. SeMet co-exposure ameliorated but did not prevent changes in telencephalon cell body density. In summary, MeHg affected both learning and brain structure, but SeMet only partially reversed the latter.
Acute effects of copper and mercury on the estuarine fish Pomatoschistus microps: Linking biomarkers to behaviour
2009, Chemosphere
The main objective of the present study was to investigate possible links between biomarkers and swimming performance in the estuarine fish Pomatoschistus microps acutely exposed to metals (copper and mercury). In independent bioassays, P. microps juveniles were individually exposed for 96 h to sub-lethal concentrations of copper or mercury. At the end of the assays, swimming performance of fish was measured using a device specially developed for epibenthic fish (SPEDE). Furthermore, the following biomarkers were measured: lipid peroxidation (LPO) and the activity of the enzymes acetylcholinesterase (AChE), lactate dehydrogenase (LDH), glutathione S-transferases (GST), 7-ethoxyresorufin-O-deethylase (EROD), superoxide dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GPx). LC₅₀s of copper and mercury (dissolved throughout metal concentrations) at 96 h were 568 μg L⁻¹ and 62 μg L⁻¹, respectively. Significant and concentration-dependent effects of both metals on swimming resistance and covered distance against water flow were found at concentrations equal or higher than 50 μg L⁻¹ for copper and 3 μg L⁻¹ for mercury (dissolved throughout metal concentrations). These results indicate that SPEDE was efficacious to quantify behavioural alterations in the epibenthic fish P. microps at ecologically relevant concentrations. Significant alterations by both metals on biomarkers were found including: inhibition of AChE and EROD activities, induction of LDH, GST and anti-oxidant enzymes, and increased LPO levels, with LOEC values ranging from 25 to 200 μg L⁻¹ for copper and from 3 to 25 μg L⁻¹ for mercury (dissolved throughout metal concentrations). Furthermore, significant and positive correlations were found between some biomarkers (AChE and EROD) and behavioural parameters, while negative correlations were found for others (LPO, anti-oxidant enzymes and LDH) suggesting that disruption of cholinergic function through AChE inhibition, decreased detoxification capability due to EROD inhibition, additional energetic demands to face chemical stress, and oxidative stress and damage may contribute to decrease the swimming performance of fish. Since a reduced swimming capability of fish may reduce their ability to capture preys, avoid predators, and interfere with social and reproductive behaviour, the exposure of P. microps to copper and/or mercury concentrations similar to those tested here may decrease the fitness of wild populations of this species.

View all citing articles on Scopus

View full text

Regular ArticleAcute Effects of Mercuric Chloride on the Olfactory Epithelium of Trichomycterus brasiliensis

Abstract

Regular Article
Acute Effects of Mercuric Chloride on the Olfactory Epithelium of Trichomycterus brasiliensis