Effects of vitamins E and A on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced lipid peroxidation and other biochemical changes in the rat

Hassan, Mohammad Q.; Stohs, Sidney J.; Murray, Wallace J.

doi:10.1007/bf01055529

Cited by 18 publications

(11 citation statements)

References 26 publications

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“…BHA has also been shown to partially restore the glutathione peroxidase activity and to block the enhanced aryl hydrocarbon hydroxylase activity as well as body, liver, and thymus weight losses produced by TCDD (Hassan et al 1987a). Previous studies have also shown that the administration of vitamin E (ct-tocopherol) to rats inhibits TCDD-induced lipid peroxidation and extends survival (Hassan et al 1987b), providing further support for the role of ROS in the toxicity of TCDD.…”

Section: Discussionmentioning

confidence: 91%

Stimulation of NADPH-dependent reactive oxygen species formation and DNA damage by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat peritoneal lavage cells

Alsharif

Schlueter

Stohs

1994

Arch. Environ. Contam. Toxicol.

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The toxicity of 2,3,7,8-tetrachlorodibenzo-p-dioxin [TCDD] and its congeners involves binding to a specific TCDD [Ah] receptor, interaction of this complex with chromatin, and the ultimate production of pleiotropic responses. The mechanism whereby these effects are produced following interaction of TCDD with the receptor complex is not known. Oxidative stress following the production of reactive oxygen species (ROS) may play an important role in the toxic manifestations of TCDD. Thus, the dose and time-dependent effects of TCDD on the production of superoxide anion by peritoneal lavage cells (primarily macrophages) from rats were examined. A maximum increase in superoxide anion production occurred on day 1 after treatment in rats with 50 and 125 micrograms TCDD/kg. At 6 h after a single dose of 125 micrograms TCDD/kg, a 2.4-fold increase in superoxide anion production was observed in peritoneal lavage cells from rats. A single dose of 5 micrograms TCDD/kg had no effect on superoxide anion production by peritoneal lavage cells. A significant increase in DNA single strand breaks within peritoneal lavage cells occurred at 12 h after the oral administration of 50 micrograms TCDD/kg, and a maximum increase in DNA single strand breaks was observed on days 3-5 after treatment. No DNA damage was detected at a dose of 5 micrograms TCDD/kg. No difference was observed with respect to dose and time in the composition of the peritoneal lavage cells. The results clearly indicate that the oral administration of TCDD activates peritoneal lavage cells in rats, and that the activation precedes the formation of DNA single strand breaks.(ABSTRACT TRUNCATED AT 250 WORDS)

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Section: Discussionmentioning

confidence: 91%

Stimulation of NADPH-dependent reactive oxygen species formation and DNA damage by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat peritoneal lavage cells

Alsharif

Schlueter

Stohs

1994

Arch. Environ. Contam. Toxicol.

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“…Daily treatment of female rats with BHA protected 100% of the animals against TCDD lethality [14]. Retinol acetate (vitamin A) and vitamin E resulted in 30% and 10% survival of a lethal dose of TCDD after 25 days [13], but did not provide long-term protection [15]. The protective effects were associated with reduced microsomal lipid peroxidation, increased glutathione peroxidase activity, and decreased aryl hydrocarbon hydroxylase activity.…”

Section: Oxidative Stress and Toxicitymentioning

confidence: 91%

“…Several of the first studies to demonstrate the possible involvement of ROS and free radicals tested the abilities of antioxidants to suppress TCDD-induced toxicity and lethality in rats. Stohs et al [13][14][15][16] treated rats with butylated hydroxyanisole (BHA), vitamin E, and retinol acetate during and after administration of a lethal dose of TCDD. Daily treatment of female rats with BHA protected 100% of the animals against TCDD lethality [14].…”

Section: Oxidative Stress and Toxicitymentioning

confidence: 99%

“…Initial studies focused on the role of the microsomal enzymes, including the cytochrome P450 system [5,[13][14][15][16], in TCDD-induced lipid peroxidation, reduction in antioxidant enzymes, and modulation of reduced glutathione levels. The dioxin-inducible AHR battery of genes contains at least six genes in mice that play important roles in the toxic effects of TCDD and its congeners, including the production of oxidative stress [43].…”

Section: Sources and Types Of Reactive Oxygen Speciesmentioning

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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“…Effective prevention of TCDD-induced toxicity by administration of antioxidants such as oltipraz[5-(2-pyrazinyl)-4-methyl-1,2-dithiol-3-thione] or butylated hydroxyanisole, or by pretreatment with vitamins A and E further supports the hypothesis that oxidative processes are involved in TCDD-induced toxicity 29,30 . Attenuation of subcellular changes in the liver and neuronal cells by transgene of TRX/ADF in the present study indicates the critical role of oxidative stress in the toxic events induced by TCDD, and also the protective function of ADF/TRX in these organs, as in our previous study of TCDD-induced bone marrow toxicity 26 .…”

Section: Discussionmentioning

confidence: 64%

Electron Microscopical Evidence of the Protective Function of Thioredoxin (TRX/ADF) Transgene against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced Cellular Toxicity in the Liver and Brain

Yoon

Kaneko²,

Hirabayashi³

et al. 2005

J Toxicol Pathol

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Abstract:The present study was performed to assess the protective role of thioredoxin/adult T-cell leukemia-derived factor (TRX/ADF) on the liver and brain cell damages induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in ADF wild-type (WT) and transgenic (Tg) mice. The ADF WT and Tg mice were intraperitoneally injected with a single dose of TCDD (150 µg/kg body weight). One day after the treatment, the liver and brain tissues were examined electron microscopically to evaluate the cellular toxicity. In the ADF WT mice, marked reduction of subcellular components, such as mitochondria, rough endoplasmic reticula, and glycogen granules, as well as swelling of the remaining mitochondria, were evident in the liver cells. However, attenuation of these changes was evident in TCDD-treated TRX/ ADF mice. Similar subcellular changes noted in the neuronal cells of TCDD-treated WT mice were also attenuated in Tg mice. The results suggest that oxidative cellular damage contributes to the acute toxicity induced by TCDD and that TRX/ADF protects against it. (J Toxicol Pathol 2005; 18: 41-46)

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Effects of vitamins E and A on 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced lipid peroxidation and other biochemical changes in the rat

Cited by 18 publications

References 26 publications

Stimulation of NADPH-dependent reactive oxygen species formation and DNA damage by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat peritoneal lavage cells

Stimulation of NADPH-dependent reactive oxygen species formation and DNA damage by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat peritoneal lavage cells

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

Electron Microscopical Evidence of the Protective Function of Thioredoxin (TRX/ADF) Transgene against 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced Cellular Toxicity in the Liver and Brain

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