Toxicity of Industrially Relevant Chlorinated Organic Solvents In Vitro

McDermott, Catherine; Heffron, J. J. A.

doi:10.1177/1091581813482006

Cited by 19 publications

(8 citation statements)

References 41 publications

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“…The authors reported a significant increase of apoptosis in the collected blood samples in association with a significant up-regulation of pro-apoptotic P53 and Bax ( Varshney et al, 2015 ). In addition, TCE exposure remarkably interferes with mitochondrial signaling through activation of caspase-dependent apoptotic cell death ( McDermott and Heffron, 2013 ) which supports the current findings.…”

Section: Resultssupporting

confidence: 88%

Toxic Effects of Trichloroethylene on Rat Neuroprogenitor Cells

et al. 2018

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Trichloroethylene (TCE) is a common volatile organic solvent which is considered as an ubiquitous environmental pollutant. It is claimed to be a developmental neurotoxicant. Our group evaluated previously its impact on three-dimensional neurospheres in vitro. The current work aims to investigate the neurotoxic effects of a lower concentration of TCE on the same system. To perform the experiment, neural progenitor cells were obtained from the brains of nine newborn rats. Afterward, these cells were cultured in both growth and differentiation media to get the neurospheres. Cell cultures were divided into two groups: group 1 (control), group 2 (exposed to 0.25 μM TCE). Neurospheres were photographed at different durations and assessment of the morphological changes such as proliferation and differentiation of neurospheres was done. In addition, cell viability, apoptosis, and necrosis were analyzed using flow cytometry to clarify the mechanism of involved cytotoxicity. The results revealed that TCE-treated neurospheres showed significantly decreased proliferation on days 7 and 14. These cells failed to show the neurogenic differentiation seen in the neurospheres of the control group. Furthermore, a highly significant decrease in viability and a significant increase in the number of apoptotic cells were observed in the treated cells in comparison to the control group. The present work confirmed that TCE, at very low doses relevant to daily life exposure in humans, caused neurotoxic effects in 3D neurosphere model through the affection of neural proliferation and differentiation as well as disturbance of cell viability and apoptosis.

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Section: Resultssupporting

confidence: 88%

Toxic Effects of Trichloroethylene on Rat Neuroprogenitor Cells

et al. 2018

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“…A significant up-regulation of pro-apoptotic P53 and its downstream target Bax was indicated in the workers blood samples (Varshney et al 2015). Moreover, TCE D r a f t exposure significantly intervened in mitochondrial signaling by activation of caspase and 3 dependent cell apoptosis (McDermott and Heffron 2013;Shen et al 2009).…”

Section: R a F Tmentioning

confidence: 94%

Developmental neurotoxic effects of a low dose of TCE on a 3-D neurosphere system

Abdraboh

Abdeen

Salama

et al. 2018

Biochem. Cell Biol.

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Trichloroethylene (TCE) is one of the industrial toxic byproducts that now persist in the air, soil, and water. Several studies have already illustrated the toxic effect of high doses of TCE on the biological functions of several organs. This study aims to highlight the toxic impact of a low dose of TCE (1 μmol/L) on the development of rat neural stem cells (NSCs). The subventricular zones (SVZ) of rat pup's brains were collected and minced, and the harvested cells were cultured in the presence of neural growth factors B27/N2 to develop neurospheres. The cells were then exposed to a dose of 1 μmol/L TCE for 1 or 2 weeks. The outcomes indicated a remarkable inhibitory effect of TCE on the differentiation capacity of NSCs, which was confirmed by down-regulation of the astrocyte marker GFAP The inhibitory effect of TCE on the proliferation of NSCs was identified by the reductions in neurosphere diameter, Ki67 expression, and cell cycle arrest at the G1/S phase. Immunolabelling with annexin V indicated the proapoptotic effect of TCE exposure. PCR results revealed a TCE-mediated suppression of the expression of the antioxidant enzyme SOD1. This paper illustrates, for the first time, a detailed examination of the toxic effects of an environmentally low dose of TCE on NCSs at the transcriptional, translational, and functional levels.

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“…Одна из актуальных медико-биологических проблем -изучение повреждающего действия экотоксикантов на организм человека. К числу этих соединений относится и дихлорэтан (ДХЭ), широко применяемый в производстве хлорвинила и полихлорвиниловой продукции в качестве растворителя отравляющих веществ, для обезжиривания и чистки одежды [1][2][3].…”

Section: экспериментальная медицинаunclassified

“…Острые отравления ДХЭ при авариях на химических производствах характеризуются высокой смертностью [1]. При этом попадание ДХЭ в почву, воду и воздух, а также длительный контакт в процессе работы на производстве могут приводить к хронической интоксикации ДХЭ [1][2][3]. Проникая в организм человека через неповреждённые кожные покровы, дыхательные пути, пищеварительный тракт, ДХЭ оказывает плейотропное повреждающее действие [1,2,4,5].…”

Section: экспериментальная медицинаunclassified

Impact of dichloroethane on the microbicidal activity of neutrophils and mononuclear phagocytes

et al. 2017

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Aim. To study the damaging effect of dichloroethane on the functional state of neutrophils and peritoneal macrophages. Methods. Dichloroethane was administered to animals intragastrically daily in olive oil at a dose of 0.84 mg/kg of body weight for 60 days so that the total dose was 0.1 of 50% lethal dose. The number of leukocytes, neutrophils and lymphocytes in peripheral blood, intensity of oxygen-dependant metabolism (induced test with nitro blue tetrazolium), antimicrobial activity in the conditions of functioning and blockade (by sodium azide), oxygen-dependent factors of microbicidity, content of myeloperoxidase and cationic proteins in neutrophils and peritoneal macrophages were measured. The results were recorded the next day after introduction of the toxicant. Fungicidal activity was measured by the number of colony-forming units of C. albicans, growing on day 3 at culture medium. Results. Intoxication with dichloroethane for 60 days leads to the formation of leukopenia, mainly due to the decreased number of neutrophils while reducing the number of lymphocytes. This is accompanied by inhibition of oxygen-dependant killing of neutrophils as a result of suppression of peroxidase-dependant mechanisms of microbicidity (the formation of oxygen active forms decreases). Besides, decrease of activity of oxygen-independant mechanisms of killing develops, which correlates with a reduction of cationic proteins level. Suppression of oxidative and non-oxidative mechanisms of microbicidity of peritoneal macrophages. This is accompanied by a decrease of oxygen-dependant metabolism intensity, myeloperoxidase activity and cationic protein level in these cells. Conclusion. Intoxication with dichloroethane for 60 days in a total dose of 0.1 of 50% lethal dose has a profound damaging effect on the cells of phagocytic link of nonspecific resistance: formation of leukopenia, suppression of oxidative metabolism and microbicidal activity of neutrophils and mononuclear phagocytes occur.

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Toxicity of Industrially Relevant Chlorinated Organic Solvents In Vitro

Cited by 19 publications

References 41 publications

Toxic Effects of Trichloroethylene on Rat Neuroprogenitor Cells

Toxic Effects of Trichloroethylene on Rat Neuroprogenitor Cells

Developmental neurotoxic effects of a low dose of TCE on a 3-D neurosphere system

Impact of dichloroethane on the microbicidal activity of neutrophils and mononuclear phagocytes

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