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      MeHg Causes Ultrastructural Changes in Mitochondria and Autophagy in the Spinal Cord Cells of Chicken Embryo

      , 1 , 2 , 2

      Journal of Toxicology

      Hindawi

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          Abstract

          Methylmercury (MeHg) is a known neurodevelopmental toxicant, which causes changes in various structures of the central nervous system (CNS). However, ultrastructural studies of its effects on the developing CNS are still scarce. Here, we investigated the effect of MeHg on the ultrastructure of the cells in spinal cord layers. Chicken embryos at E3 were treated in ovo with 0.1 μg MeHg/50 μL saline solution and analyzed at E10. Then, we used transmission electron microscopy (TEM) to identify possible damage caused by MeHg to the structures and organelles of the spinal cord cells. After MeHg treatment, we observed, in the spinal cord mantle layer, a significant number of altered mitochondria with external membrane disruptions, crest disorganization, swelling in the mitochondrial matrix, and vacuole formation between the internal and external mitochondrial membranes. We also observed dilations in the Golgi complex and endoplasmic reticulum cisterns and the appearance of myelin-like cytoplasmic inclusions. We observed no difference in the total mitochondria number between the control and MeHg-treated groups. However, the MeHg-treated embryos showed an increased number of altered mitochondria and a decreased number of mitochondrial fusion profiles. Additionally, unusual mitochondrial shapes were found in MeHg-treated embryos as well as autophagic vacuoles similar to mitophagic profiles. In addition, we observed autophagic vacuoles with amorphous, homogeneous, and electron-dense contents, similar to the autophagy. Our results showed, for the first time, the neurotoxic effect of MeHg on the ultrastructure of the developing spinal cord. Using TEM we demonstrate that changes in the endomembrane system, mitochondrial damage, disturbance in mitochondrial dynamics, and increase in mitophagy were caused by MeHg exposure.

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          Most cited references 85

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          Mitochondrial fission, fusion, and stress.

          Mitochondrial fission and fusion play critical roles in maintaining functional mitochondria when cells experience metabolic or environmental stresses. Fusion helps mitigate stress by mixing the contents of partially damaged mitochondria as a form of complementation. Fission is needed to create new mitochondria, but it also contributes to quality control by enabling the removal of damaged mitochondria and can facilitate apoptosis during high levels of cellular stress. Disruptions in these processes affect normal development, and they have been implicated in neurodegenerative diseases, such as Parkinson's.
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            Impairment of starvation-induced and constitutive autophagy in Atg7-deficient mice

            Autophagy is a membrane-trafficking mechanism that delivers cytoplasmic constituents into the lysosome/vacuole for bulk protein degradation. This mechanism is involved in the preservation of nutrients under starvation condition as well as the normal turnover of cytoplasmic component. Aberrant autophagy has been reported in several neurodegenerative disorders, hepatitis, and myopathies. Here, we generated conditional knockout mice of Atg7, an essential gene for autophagy in yeast. Atg7 was essential for ATG conjugation systems and autophagosome formation, amino acid supply in neonates, and starvation-induced bulk degradation of proteins and organelles in mice. Furthermore, Atg7 deficiency led to multiple cellular abnormalities, such as appearance of concentric membranous structure and deformed mitochondria, and accumulation of ubiquitin-positive aggregates. Our results indicate the important role of autophagy in starvation response and the quality control of proteins and organelles in quiescent cells.
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              Critical periods of vulnerability for the developing nervous system: evidence from humans and animal models.

               Greg Rice,  S Barone (2000)
              Vulnerable periods during the development of the nervous system are sensitive to environmental insults because they are dependent on the temporal and regional emergence of critical developmental processes (i.e., proliferation, migration, differentiation, synaptogenesis, myelination, and apoptosis). Evidence from numerous sources demonstrates that neural development extends from the embryonic period through adolescence. In general, the sequence of events is comparable among species, although the time scales are considerably different. Developmental exposure of animals or humans to numerous agents (e.g., X-ray irradiation, methylazoxymethanol, ethanol, lead, methyl mercury, or chlorpyrifos) demonstrates that interference with one or more of these developmental processes can lead to developmental neurotoxicity. Different behavioral domains (e.g., sensory, motor, and various cognitive functions) are subserved by different brain areas. Although there are important differences between the rodent and human brain, analogous structures can be identified. Moreover, the ontogeny of specific behaviors can be used to draw inferences regarding the maturation of specific brain structures or neural circuits in rodents and primates, including humans. Furthermore, various clinical disorders in humans (e.g., schizophrenia, dyslexia, epilepsy, and autism) may also be the result of interference with normal ontogeny of developmental processes in the nervous system. Of critical concern is the possibility that developmental exposure to neurotoxicants may result in an acceleration of age-related decline in function. This concern is compounded by the fact that developmental neurotoxicity that results in small effects can have a profound societal impact when amortized across the entire population and across the life span of humans. Images Figure 2 Figure 3 Figure 4 Figure 5 Figure 6 Figure 8 Figure 9 Figure 12 Figure 14 Figure 16 Figure 17
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                Author and article information

                Contributors
                Journal
                J Toxicol
                J Toxicol
                JT
                Journal of Toxicology
                Hindawi
                1687-8191
                1687-8205
                2018
                28 August 2018
                : 2018
                Affiliations
                1Instituto de Ciências Naturais Humanas e Sociais, UFMT, Avenida Alexandre Ferronato 1200, Setor Industrial, Sinop, MT 78557287, Brazil
                2Departamento de Biologia Celular, Embriologia e Genética, Centro de Ciências Biológicas, UFSC, Campus Universitário, Trindade, Florianópolis, SC 88040-900, Brazil
                Author notes

                Academic Editor: Brad Upham

                10.1155/2018/8460490
                6136469
                Copyright © 2018 Fabiana F. Ferreira et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Categories
                Research Article

                Toxicology

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