“…Although the content of Cd in water is strictly monitored all over the world, its concentrations still exceed the standard in many areas. The latest surveys revealed that the concentrations of Cd 2+ range from 0.1 to 0.3 μg/L in various water systems and can even reach 300 μg/L in polluted rivers [ 7 , 8 , 9 , 10 ]. Specifically, the concentration of Cd in groundwater around waste disposal sites in the United States is as high as 6000 μg/L and leachates from municipal solid waste landfills in the European Union can reach up to 2700 μg/L [ 11 , 12 ].…”
Cadmium (Cd) is a toxic heavy metal and worldwide environmental pollutant which seriously threatens human health and ecosystems. It is easy to be adsorbed and deposited in organisms, exerting adverse effects on various organs including the brain. In a very recent study, making full use of a zebrafish model in both high-throughput behavioral tracking and live neuroimaging, we explored the potential developmental neurotoxicity of Cd2+ at environmentally relevant levels and identified multiple connections between Cd2+ exposure and neurodevelopmental disorders as well as microglia-mediated neuroinflammation, whereas the underlying neurotoxic mechanisms remained unclear. The canonical Wnt/β-catenin signaling pathway plays crucial roles in many biological processes including neurodevelopment, cell survival, and cell cycle regulation, as well as microglial activation, thereby potentially presenting one of the key targets of Cd2+ neurotoxicity. Therefore, in this follow-up study, we investigated the implication of the Wnt/β-catenin signaling pathway in Cd2+-induced developmental disorders and neuroinflammation and revealed that environmental Cd2+ exposure significantly affected the expression of key factors in the zebrafish Wnt/β-catenin signaling pathway. In addition, pharmacological intervention of this pathway via TWS119, which can increase the protein level of β-catenin and act as a classical activator of the Wnt signaling pathway, could significantly repress the Cd2+-induced cell cycle arrest and apoptosis, thereby attenuating the inhibitory effects of Cd2+ on the early development, behavior, and activity, as well as neurodevelopment of zebrafish larvae to a certain degree. Furthermore, activation and proliferation of microglia, as well as the altered expression profiles of genes associated with neuroimmune homeostasis triggered by Cd2+ exposure could also be significantly alleviated by the activation of the Wnt/β-catenin signaling pathway. Thus, this study provided novel insights into the cellular and molecular mechanisms of Cd2+ toxicity on the vertebrate central nervous system (CNS), which might be helpful in developing pharmacotherapies to mitigate the neurological disorders resulting from exposure to Cd2+ and many other environmental heavy metals.
“…Although the content of Cd in water is strictly monitored all over the world, its concentrations still exceed the standard in many areas. The latest surveys revealed that the concentrations of Cd 2+ range from 0.1 to 0.3 μg/L in various water systems and can even reach 300 μg/L in polluted rivers [ 7 , 8 , 9 , 10 ]. Specifically, the concentration of Cd in groundwater around waste disposal sites in the United States is as high as 6000 μg/L and leachates from municipal solid waste landfills in the European Union can reach up to 2700 μg/L [ 11 , 12 ].…”
Cadmium (Cd) is a toxic heavy metal and worldwide environmental pollutant which seriously threatens human health and ecosystems. It is easy to be adsorbed and deposited in organisms, exerting adverse effects on various organs including the brain. In a very recent study, making full use of a zebrafish model in both high-throughput behavioral tracking and live neuroimaging, we explored the potential developmental neurotoxicity of Cd2+ at environmentally relevant levels and identified multiple connections between Cd2+ exposure and neurodevelopmental disorders as well as microglia-mediated neuroinflammation, whereas the underlying neurotoxic mechanisms remained unclear. The canonical Wnt/β-catenin signaling pathway plays crucial roles in many biological processes including neurodevelopment, cell survival, and cell cycle regulation, as well as microglial activation, thereby potentially presenting one of the key targets of Cd2+ neurotoxicity. Therefore, in this follow-up study, we investigated the implication of the Wnt/β-catenin signaling pathway in Cd2+-induced developmental disorders and neuroinflammation and revealed that environmental Cd2+ exposure significantly affected the expression of key factors in the zebrafish Wnt/β-catenin signaling pathway. In addition, pharmacological intervention of this pathway via TWS119, which can increase the protein level of β-catenin and act as a classical activator of the Wnt signaling pathway, could significantly repress the Cd2+-induced cell cycle arrest and apoptosis, thereby attenuating the inhibitory effects of Cd2+ on the early development, behavior, and activity, as well as neurodevelopment of zebrafish larvae to a certain degree. Furthermore, activation and proliferation of microglia, as well as the altered expression profiles of genes associated with neuroimmune homeostasis triggered by Cd2+ exposure could also be significantly alleviated by the activation of the Wnt/β-catenin signaling pathway. Thus, this study provided novel insights into the cellular and molecular mechanisms of Cd2+ toxicity on the vertebrate central nervous system (CNS), which might be helpful in developing pharmacotherapies to mitigate the neurological disorders resulting from exposure to Cd2+ and many other environmental heavy metals.
“…The apple snail Pomacea canaliculata has emerged as a possible bioindicator of elemental pollution ( Adewunmi et al, 1996 ; Ezemonye et al, 2006 ; Deng et al, 2008 ; Vega et al, 2012 ; Campoy-Diaz et al, 2018 ; Campoy-Diaz et al, 2020 ) due to its worldwide distribution in humid tropical and subtropical freshwater ecosystems ( Hayes et al, 2015 ), can be cultured and kept under laboratory-controlled conditions, and their tissues can accumulate a diverse array of ecologically relevant elements (e.g. As, Cd, Cu, Hg, Pb, U, Zn) ( Callil and Junk, 2001 ; Peña and Pocsidio, 2008 ; Vega et al, 2012 ; Campoy-Diaz et al, 2018 ; Huang et al, 2018 ; Campoy-Diaz et al, 2020 ; Juarez et al, 2022 ). Furthermore, the digestive gland and symbionts from P. canaliculata participate in metal accumulation.…”
Section: Introductionmentioning
confidence: 99%
“…Furthermore, the digestive gland and symbionts from P. canaliculata participate in metal accumulation. Additionally, these symbionts are involved in metal depuration ( Castro-Vazquez et al, 2002 ; Vega et al, 2005 ; Vega et al, 2006 ; Vega et al, 2012 ; Campoy-Diaz et al, 2018 ; Campoy-Diaz et al, 2020 ) when are expelled in the feces ( Koch et al, 2006 ). However, our knowledge about the physiological response of the digestive gland to different prooxidant elements remains incomplete.…”
The freshwater gastropod Pomacea canaliculata fulfills the ideal conditions of a bioindicator species since its digestive gland bioconcentrates elements toxic for human and ecosystems health. The aim of this work was to study the balance between production of free radicals and antioxidant defenses, and the generation of oxidative damage in the digestive gland of this mollusk after exposure (96 h) to three elements with differential affinities for functional biological groups: mercury (5.5 μg/L of Hg+2 as HgCl2), arsenic [500 μg/L of (AsO4)−3 as Na3AsO47H2O], or uranium [700 μg/L of (UO2)+2 as UO2(CH2COOH)2]. Bioconcentration factors of Hg, As, and U were 25, 23, and 53, respectively. Snails exhibited a sustained increase of reactive species (RS), and protein and lipid damage. Lipid radicals increased between 72 and 96 h, respectively, in snails exposed to U and Hg while this parameter changed early (24 h) in As- exposed snails. Snails showed protein damage, reaching maximum values at different endpoints. This redox disbalance was partially compensated by non-enzymatic antioxidant defenses α-tocopherol (α-T), β-carotene (β-C), uric acid, metallothionein (MTs). Snails consumed α-T and β-C in an element-dependent manner. The digestive gland consumed rapidly uric acid and this molecule was not recovered at 96 h. Digestive gland showed a significant increase in MTs after elemental exposure at different endpoints. The enzymatic antioxidant defenses, represented by the catalase and glutathione-S-transferase activities, seems to be not necessary for the early stages of the oxidative process by metals. This work is the first attempt to elucidate cellular mechanisms involved in the tolerance of this gastropod to non-essential elements. The bioconcentration factors and changes in the oxidative status and damage confirm that this species can be used as a bioindicator species of metal pollution in freshwater bodies.
“…Likewise, some field and laboratory studies have shown that representatives of the genus Pomacea may be useful for environmental risk assessment of diverse chemical pollutants in nature, i.e., elements (arsenic, As; cadmium, Cd; copper, Cu; mercury, Hg; lead, Pb; uranium, U; zinc, Zn) [10,[17][18][19][20][21], the herbicide glyphosate [22], the insecticides cypermethrin, bifentrin and imidacloprid [23,24]. On the other hand, under controlled laboratory conditions, organotin compounds cause a masculinizing effect on adult (4 months old) females of P. canaliculata [25,26].…”
All female Pomacea canaliculata develop a small, male-like copulatory apparatus a few days after birth, which growths slowly until sexual maturity, and even further in older age. Previous studies have found trace elements like mercury (Hg), arsenic (As) and uranium (U) in tap water used for snail culture, and that these elements were accumulated in snail tissues. Here, we test whether the presence of these metals at maximum allowed concentrations (Environmental Protection Agency - EPA) in aquarium water could affect the development of the copulatory apparatus in mature females. Females of different ages were used as controls, grown in reconstituted metal-free water with or without the addition of Hg, As and U, as well as tributyltin (TBT), a compound used as masculinizing agent. Six and seven months old females cultured in tap water showed a longer penis and penile sheath, and a greater overall development of the copulatory apparatus, measured by an index (DI), as compared with same-age females cultured in reconstituted water. Moreover, when females were exposed to Hg, As or U at the maximum contaminant levels for human consumption allowed by EPA regulations, there was no further development of the copulatory apparatus, while there was a clearly positive effect in TBT-exposed females. This study confirms the masculinizing effect of organotin compounds on female copulatory apparatus and discusses the usefulness of the development of these organs as a bioindicator of environmental pollution.
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