Trichloroethylene accelerates an autoimmune response by Th1 T cell activation in MRL+/+ mice

Griffin, Joseph M.; Blossom, Sarah J.; Jackson, Stephanie K.; Gilbert, Kathleen M.; Pumford, Neil R.

doi:10.1016/s0162-3109(99)00164-2

Cited by 99 publications

(94 citation statements)

References 35 publications

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“…TCE-treated groups showed a significant increase in the liver MDA level in comparison to untreated groups. TCE insult also led to increased formation of MDA in sera, spleens and kidneys, major organs where TCE is known to generate free radicals and induce autoimmune disorders (Griffin et al, 2000;Wang et al, 2013), further confirming earlier findings of the potential of TCE in inducing increased lipid peroxidation. It was found that the TCE treatment can result in hepatotoxicity by elevating the oxidative stress markers MDA, hydroxynonenal (HNE)-protein, and protein oxidation (carbonylation) (Wang et al, 2013).…”

Section: Tce Induces Vascular and Degenerative Changes In Hepatic Arcsupporting

confidence: 87%

“…4b). Discussion The exposure to environmental toxic chemicals can cause several detrimental effects in biological cell systems (Topham, 1980;House et al, 1996;Snyder and Andrews, 1996;Griffin et al, 2000;Wang et al, 2007Wang et al, , 2013Al-Griw et al, 2015a,b,c). TCE, a widely used industrial agent and a ubiquitous environmental contaminant, is non-carcinogenic (group 3) because there is inadequate evidence for carcinogenicity in both human and animals according to EPA and National Toxicology Program (NTP) technical report (NTP, 2000;EPA, 2007).…”

Section: Tce Induces Vascular and Degenerative Changes In Hepatic Arcmentioning

confidence: 99%

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Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality

Al-Griw¹,

Alghazeer²,

Al-Azreg³

et al. 2016

Open Vet J.

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Exposures to a wide variety of environmental substances are negatively associated with many biological cell systems both in humans and rodents. Trichloroethane (TCE), a ubiquitous environmental toxicant, is used in large quantities as a dissolvent, metal degreaser, chemical intermediate, and component of consumer products. This increases the likelihood of human exposure to these compounds through dermal, inhalation and oral routes. The present in vivo study was aimed to investigate the possible cellular and molecular etiology of liver abnormality induced by early exposure to TCE using a murine model. The results showed a significant increase in liver weight. Histopathological examination revealed a TCE-induced hepatotoxicity which appeared as heavily congested central vein and blood sinusoids as well as leukocytic infiltration. Mitotic figures and apoptotic changes such as chromatin condensation and nuclear fragments were also identified. Cell death analysis demonstrates hepatocellular apoptosis was evident in the treated mice compared to control. TCE was also found to induce oxidative stress as indicated by an increase in the levels of lipid peroxidation, an oxidative stress marker. There was also a significant decrease in the DNA content of the hepatocytes of the treated groups compared to control. Agarose gel electrophoresis also provided further biochemical evidence of apoptosis by showing internucleosomal DNA fragmentation in the liver cells, indicating oxidative stress as the cause of DNA damage. These results suggest the need for a complete risk assessment of any new chemical prior to its arrival into the consumer market.

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Section: Tce Induces Vascular and Degenerative Changes In Hepatic Arcsupporting

confidence: 87%

Section: Tce Induces Vascular and Degenerative Changes In Hepatic Arcmentioning

confidence: 99%

Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality

Al-Griw¹,

Alghazeer²,

Al-Azreg³

et al. 2016

Open Vet J.

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“…By using a female MRL+/+ mouse model, we have shown that chronic exposure to TCE during adulthood promotes autoimmune hepatitis that corresponds to idiopathic autoimmune hepatitis in humans, that is, T-cell infiltration of the liver and development of antibodies specific for liver microsomal proteins [15,16]. TCE exposure appears to predominantly impact CD4 + T cells, with effects on cellularity manifested as increased percentages of effector/memory CD4 + T cells with altered cytokine production profiles [15,17].…”

mentioning

confidence: 99%

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

et al. 2016

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Aim: Autoimmune disease and CD4+ T-cell alterations are induced in mice exposed to the water pollutant trichloroethylene (TCE). We examined here whether TCE altered gene-specific DNA methylation in CD4 + T cells as a possible mechanism of immunotoxicity. Materials & methods: Naive and effector/memory CD4 + T cells from mice exposed to TCE (0.5 mg/ml in drinking water) for 40 weeks were examined by bisulfite next-generation DNA sequencing. Results: A probabilistic model calculated from multiple genes showed that TCE decreased methylation control in CD4 + T cells. Data from individual genes fitted to a quadratic regression model showed that TCE increased gene-specific methylation variance in both CD4 subsets. Conclusion: TCE increased epigenetic drift of specific CpG sites in CD4 + T cells.

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“…41,42) Another study examined lower TCE exposure levels (0.1, 0.5, and 2.5 mg/ml) and extended the observation to 32 weeks. 43) These studies demonstrated an acceleration of the autoimmune response.…”

Section: Animal Studiesmentioning

confidence: 99%

Immunotoxic Effects of Trichloroethylene and Tetrachloroethylene

Seo

Kobayashi

Nagase

2011

JOURNAL OF HEALTH SCIENCE

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Allergic diseases have been increasing worldwide in industrialized countries. The interplay of genetic and environmental factors is involved in the induction and progression of several types of allergic diseases. Recently, there have been many reports that the increase and spread of allergic diseases are related to chronic exposure to several environmental pollutants, such as diesel exhaust particles and formaldehyde. Trichloroethylene (TCE) and tetrachloroethylene (PCE) are categorized into chlorinated organic compounds, and are the most widely used extensively in various industrial processes. As a consequence of their widespread use, TCE and PCE are becoming environmental pollutants. Generally, TCE and PCE exposure causes organ toxicological effects on the liver, kidney, and the central nervous system; however, studies of TCE and PCE exposure-induced immune modulations are limited. In this review, we summarize research into immunotoxic effects, such as allergy hypersensitivity, autoimmune disease, and immunosuppression, of TCE and PCE from experimental animal studies and human epidemiological studies.

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Trichloroethylene accelerates an autoimmune response by Th1 T cell activation in MRL+/+ mice

Cited by 99 publications

References 35 publications

Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality

Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells

Immunotoxic Effects of Trichloroethylene and Tetrachloroethylene

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Trichloroethylene accelerates an autoimmune response by Th1 T cell activation in MRL+/+ mice

Cited by 99 publications

References 35 publications

Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality

Cellular and molecular etiology of hepatocyte injury in a murine model of environmentally induced liver abnormality

Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 + T cells

Immunotoxic Effects of Trichloroethylene and Tetrachloroethylene

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Chronic Exposure to Water Pollutant Trichloroethylene Increased Epigenetic Drift in CD4 ⁺ T cells