Induction of Oxidative Stress in Brain Tissues of Mice after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-<i>p</i>-dioxin

Hassoun, Ezdihar A.; Wilt, Shawn C.; DeVito, Michael J.; Birgelen, Angelique Van; Alsharif, Naser Z.; Birnbaum, Linda S.; Stohs, Sidney J.

doi:10.1093/toxsci/42.1.23

Cited by 58 publications

(24 citation statements)

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“…A series of more detailed studies on the induction of oxidative stress in brain tissues have been conducted by Hassoun et al [20,84,98,[123][124][125][126]. Oral administration of up to 150 ng TCDD/kg/day to female mice for 13 weeks resulted in dose-dependent increases in whole brain superoxide anion, lipid peroxidation, and DNA single-strand breaks [123].…”

Section: Oxidative Stress and Neurotoxicitymentioning

confidence: 99%

“…Oral administration of up to 150 ng TCDD/kg/day to female mice for 13 weeks resulted in dose-dependent increases in whole brain superoxide anion, lipid peroxidation, and DNA single-strand breaks [123]. The subchronic exposure of female rats to low doses of TCDD and two of its congeners, PeCDF and PCB126, produced dose-dependent increases in brain superoxide anion, lipid peroxidation, and DNA single-strand breaks [98].…”

Section: Oxidative Stress and Neurotoxicitymentioning

confidence: 99%

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Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Stohs

Hassoun

2011

The AH Receptor in Biology and Toxicology

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Section: Oxidative Stress and Neurotoxicitymentioning

confidence: 99%

Section: Oxidative Stress and Neurotoxicitymentioning

confidence: 99%

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Stohs

Hassoun

2011

The AH Receptor in Biology and Toxicology

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“…1) Recent studies have demonstrated that oxidative stress is an important constituent in the mechanism of TCDD toxicity. 2,3) The increased production of reactive oxygen species, lipid peroxidation, and DNA and membrane damage are always associated with TCDD exposure. 4) Several studies have suggested that TCDD causes the activation of the aryl hydrocarbon receptor (AhR), which is a ligand-activated transcription factor in most cell and tissue types.…”

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confidence: 99%

Protective Effects of Tea Melanin against 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Toxicity: Antioxidant Activity and Aryl Hydrocarbon Receptor Suppressive Effect

Hung

Huang

Sava

et al. 2006

Biological & Pharmaceutical Bulletin

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We examined the protective ability of tea melanin against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced toxicity in C57BL6J mice. Reduced tea melanin (RTM) and non-reduced tea melanin (NRTM) were incorporated to distinguish anti-oxidant activity from alternative pathways. The mice were given a single oral dose of TCDD (100 m mg/kg body weight) and then they were administered daily with NRTM or RTM (40 mg/kg, p.o.) for next 14 d. RTM protected the animals against TCDD-induced lipid peroxidation, inhibition of glutathione peroxidase, alteration in reduced and oxidized glutathione concentrations, loss of body weight, and increased relative liver weight. NRTM was less effective as compared to RTM because of its inferior antioxidant activity, but it still displayed a strong protective effect against TCDD toxicity owing to its similar suppression of the activity of the aryl hydrocarbon receptor. Both NRTM and RTM suppressed the expression of CYP1A1 gene and prevented the activation of cytochrome P450 isozyme in the livers of animals exposed to TCDD. These results suggest that tea melanin might be a potential agent offering dual protection against the development of TCDD-induced oxidative stress.

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“…[2][3][4] Chitooligosaccharides are known to be biologically active compounds. 5) Chitohexaose and its N-peracetylated derivative were shown to inhibit the growth of murine cancer cells.…”

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confidence: 99%

Effect of Chitosan Oligosaccharide on 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Oxidative Stress in Mice.

Shon

Park

Moon

et al. 2002

Biological & Pharmaceutical Bulletin

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Polyhalogenated aromatic hydrocarbons (PAHs) are highly persistent environmental contaminants that pose a potential risk to human health. 2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is the prototypical representative of these widely dispersed pollutants and one of the most potent toxins and tumor promoters known to man. TCDD exposure in experimental animals results in an array of tissue and species-specific responses, including the following: dermal toxicity, immunotoxicity, hepatoxicity, carcinogenicity, teratogenicity, and neurobehavioral, endocrine, and metabolic alterations. 1)Recent studies have demonstrated that oxidative stress occurs in various tissues of TCDD-treated animals and is considered an important mechanism in the toxicity of TCDD. 2,3)Oxidative stress following TCDD exposure in laboratory animals has been demonstrated to increase the production of reactive oxygen species, lipid peroxidation, DNA and membrane damage, and possible enzyme inhibition. [2][3][4] Chitooligosaccharides are known to be biologically active compounds.5) Chitohexaose and its N-peracetylated derivative were shown to inhibit the growth of murine cancer cells.6) N-Acetylchitohexose protected against Candida albicans infection and increased the activities of macrophages, T lymphocytes, and natural killer cells in tumor-bearing mice. 5)The current authors previously demonstrated the effects of chitosan oligosaccharide on enzymes for cancer chemoprevention 7) and various chemical mutagens. 8,9) In this study, the effects of two types of chitosan oligosaccharides, chitosan oligosaccharide I (1-kDaϽMWϽ3-kDa) and chitosan oligosaccharide II (3-kDaϽMWϽ5-kDa), on the oxidative stress resulting from exposure to TCDD were investigated in mice. MATERIALS AND METHODS MaterialsWater soluble chitosan oligosaccharides were prepared from 1% chitosan by an ultrafiltration membrane reactor system (Millipore Minitan system; molecular weight cut-off 5000, 3000, and 1000 membrane) which recycles a chitosanase (derived from Bacillus pumilus BN-262).Animals and Treatments Five-week-old male ICR mice were purchased from the Dae-Han Laboratory Animal Research Center (Eumsung, Korea). The animals were housed ten per cage. After a one-week acclimation period, chitosan oligosaccharide I, chitosan oligosaccharide II, or the vehicle alone were administered for 14 consecutive days (intragastric application at doses of 500 mg/kg). A single dose of 25 mg TCDD/kg was administered by oral gavage with corn oil as the vehicle on day 8. At the end of the application regimen, the mice were killed by cervical dislocation. The livers were perfused with a cold 0.15 M KCl buffer (pH 7.0) and homogenized in 0.25 M sucrose. Microsomes and the cytosol fractions were prepared from liver homogenates by differential centrifugation.Determination of Lipid Peroxidation Microsomal malondialdehyde (MDA) production was used as an index of lipid peroxidation. Microsomes (300 mg/ml) were incubated at 37°C for 60 min with 0.4 mM FeSO 4 and 0.2 mM ascorbic acid in 0.1 M Tris-HCl buff...

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Induction of Oxidative Stress in Brain Tissues of Mice after Subchronic Exposure to 2,3,7,8-Tetrachlorodibenzo-p-dioxin

Cited by 58 publications

References 0 publications

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Dioxin‐Activated AHR: Toxic Responses and the Induction of Oxidative Stress

Protective Effects of Tea Melanin against 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Toxicity: Antioxidant Activity and Aryl Hydrocarbon Receptor Suppressive Effect

Effect of Chitosan Oligosaccharide on 2,3,7,8-Tetrachlorodibenzo-p-dioxin-Induced Oxidative Stress in Mice.

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