Lipid peroxidation induced by trichloroethylene in rat liver

Oginö, Kazuhíde; Tatuya, Hobara; Kobayashi, Haruo; Ishiyama, H.; Gotoh, Masayuki; Imamura, Akihisa; Egami, Norio

doi:10.1007/bf01688941

Cited by 14 publications

(9 citation statements)

References 16 publications

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“…These findings were further substantiated by others [31,32] and our follow-up studies [2,[33][34][35][36]. TCE is known to generate free radicals and induces lipid peroxidation both in vivo and in vitro [2,[35][36][37][38][39]. Our recent studies show an association between TCE-induced lipid peroxidation and induction/exacerbation of autoimmune response in MRL+/+ mice, and thus suggest that lipid peroxidation and/or LPDAprotein adducts may play an important role in the disease pathogenesis [2,35,36].…”

Section: Introductionsupporting

confidence: 87%

Lipid peroxidation-derived aldehyde–protein adducts contribute to trichloroethene-mediated autoimmunity via activation of CD4+ T cells

Wang¹,

König²,

Ansari³

et al. 2008

Free Radical Biology and Medicine

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Lipid peroxidation is implicated in the pathogenesis of various autoimmune diseases. Lipid peroxidation-derived aldehydes (LPDAs) such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE) are highly reactive and bind to proteins, but their role in eliciting an autoimmune response and contribution to disease pathogenesis remains unclear. To investigate the role of lipid peroxidation in the induction and/or exacerbation of autoimmune response, 6-week-old autoimmune-prone female MRL +/+ mice were treated for 4 weeks with trichloroethene (TCE; 10 mmol/kg, i.p., once a week), an environmental contaminant known to induce lipid peroxidation. Sera from TCE-treated mice showed significant levels of antibodies against MDA-and HNE-adducted proteins along with antinuclear antibodies. This suggested that TCE exposure not only caused increased lipid peroxidation, but also accelerated autoimmune responses. Furthermore, stimulation of cultured splenic lymphocytes from both control and TCE-treated mice with MDA-adducted mouse serum albumin (MDA-MSA) or HNE-MSA for 72 h showed significant proliferation of CD4 + T cells in TCE-treated mice as analyzed by flow cytometry. Also, splenic lymphocytes from TCE-treated mice released more IL-2 and IFN-γ into cultures when stimulated with MDA-MSA or HNE-MSA, suggesting a Th1 cell activation. Thus, our data suggest a role for lipid peroxidation-derived aldehydes in TCEmediated autoimmune responses and involvement of Th1 cell activation.

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Section: Introductionsupporting

confidence: 87%

Lipid peroxidation-derived aldehyde–protein adducts contribute to trichloroethene-mediated autoimmunity via activation of CD4+ T cells

Wang¹,

König²,

Ansari³

et al. 2008

Free Radical Biology and Medicine

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“…Experimental studies have established that TCE exposure leads to lipid peroxidation (Cojocel et al, 1989;Ogino et al, 1991;Channel et al, 1998;Khan et al, 2001). Lipid peroxidation induced by TCE has been associated with liver and kidney damage (Cojocel et al, 1989;Channel et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

“…There is considerable evidence for induction of oxidative stress as a result of TCE exposure (Ogino et al, 1991;Channel et al, 1998;Khan et al, 2001). Since oxidative and nitrosative stress could occur simultaneously, it was logical to study the possible involvement of RNS whose formation and contribution has not been studied in TCE-induced autoimmune response.…”

Section: Discussionmentioning

confidence: 99%

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Oxidative and nitrosative stress in trichloroethene-mediated autoimmune response

et al. 2007

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Reactive oxygen and nitrogen species (RONS) are implicated in the pathogenesis of several autoimmune diseases. Also, increased lipid peroxidation and protein nitration are reported in systemic autoimmune diseases. Lipid peroxidation-derived aldehydes (LPDAs) such as malondialdehyde (MDA) and 4-hydroxynonenal (HNE) are highly reactive and bind proteins covalently, but their potential to elicit an autoimmune response and contribution to disease pathogenesis remain unclear. Similarly, nitration of protein could also contribute to disease pathogenesis. To assess the status of lipid peroxidation and/or RONS, autoimmune-prone female MRL +/+ mice (5-week old) were treated with trichloroethene (TCE), an environmental contaminant known to induce autoimmune response, for 48 weeks (0.5 mg/ml via drinking water), and formation of antibodies to LPDA-protein adducts was followed in the sera of control and TCE-treated mice. TCE treatment led to greater formation of both anti-MDA-and and-HNE-protein adduct antibodies and higher serum iNOS and nitrotyrosine levels. The increase in TCE-induced oxidative stress was associated with increases in anti-nuclear-, anti-ssDNA-and anti-dsDNA-antibodies. These findings suggest that TCE exposure not only leads to oxidative/nitrosative stress, but is also associated with induction/exacerbation of autoimmune response in MRL +/+ mice. Further interventional studies are needed to establish a causal role of RONS in TCE-mediated autoimmunity.

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“…The mechanism by which developmental exposure to TCE imparts neurotoxicity is largely understudied. Several studies have shown that TCE induces oxidative stress (Ogino et al, 1991; Channel et al, 1998; Wang et al, 2009). We have focused on oxidative stress responses in the brain associated with developmental TCE exposure.…”

Section: Introductionmentioning

confidence: 99%

Inflammatory and oxidative stress-related effects associated with neurotoxicity are maintained after exclusively prenatal trichloroethylene exposure

Blossom

Melnyk

et al. 2017

NeuroToxicology

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Trichloroethylene (TCE) is a widespread environmental toxicant with immunotoxic and neurotoxic potential. Previous studies have shown that continuous developmental exposure to TCE encompassing gestation and early life as well as postnatal only exposure in the drinking water of MRL+/+ mice promoted CD4+ T cell immunotoxicity, glutathione depletion and oxidative stress in the cerebellum, as well increased locomotor activity in male offspring. The purpose of this study was to characterize the effects of exclusively prenatal exposure on these parameters. Another goal was to investigate potential plasma oxidative stress/inflammatory biomarkers to possibly be used as predictors of TCE-mediated neurotoxicity. In the current study, 6 week old male offspring of dams exposed gestationally to 0, 0.01, and 0.1 mg/ml TCE in the drinking water were evaluated. Our results confirmed that the oxidized phenotype in plasma and cerebellum was maintained after exclusively prenatal exposure. A Phenotypic analysis by flow cytometry revealed that TCE exposure expanded the effector/memory subset of peripheral CD4+ T cells in association with increased production of pro-inflammatory cytokines IFN-γ and IL-17. Serum biomarkers of oxidative stress and inflammation were also elevated in plasma suggesting that systemic effects are important and may be used to predict neurotoxicity in our model. These results suggested that the prenatal period is a critical stage of life by which the developing CNS and immune system are susceptible to long-lasting changes mediated by TCE.

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Lipid peroxidation induced by trichloroethylene in rat liver

Cited by 14 publications

References 16 publications

Lipid peroxidation-derived aldehyde–protein adducts contribute to trichloroethene-mediated autoimmunity via activation of CD4+ T cells

Lipid peroxidation-derived aldehyde–protein adducts contribute to trichloroethene-mediated autoimmunity via activation of CD4+ T cells

Oxidative and nitrosative stress in trichloroethene-mediated autoimmune response

Inflammatory and oxidative stress-related effects associated with neurotoxicity are maintained after exclusively prenatal trichloroethylene exposure

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