Induction of oxidative stress in brain tissues of mice after subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin

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

Research output: Contribution to journalArticle

58 Citations (Scopus)

Abstract

The ability of single doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to induce oxidative stress in hepatic and some extrahepatic tissues of animals is well documented. However, no previous study has examined the ability of TCDD to induce oxidative stress and tissue damage in brain in vivo. In this study the ability of TCDD to induce oxidative stress in brain tissues of mice was studied after subchronic exposures. Groups of female B6C3F1 mice were treated orally with TCDD (0, 0.45, 1.5, 15, and 150 ng/kg/day) for 13 weeks, 5 days/week. The animals were euthanized 3 days after the last treatment and brain tissues were collected. Biomarkers of oxidative stress including production of superoxide anion, lipid peroxidation, and DNA-single-strand breaks (SSB) were determined. TCDD treatment resulted in significant and dose-dependent increases in the production of superoxide anion as assessed by reduction of cytochrome c. Significant increases were also observed in lipid peroxidation and DNA-SSB in those tissues, as assessed by the presence of thiobarbituric acid-reactive substances and the alkaline elution technique, respectively. These results clearly indicate that subchronic exposure to low doses of TCDD can induce oxidative tissue damage in brain tissues which may at least in part play a role in the effects of TCDD on the central nervous system.

Original languageEnglish
Pages (from-to)23-27
Number of pages5
JournalToxicological Sciences
Volume42
Issue number1
DOIs
StatePublished - Mar 1998

Fingerprint

Oxidative stress
Brain
Oxidative Stress
Tissue
Single-Stranded DNA Breaks
Superoxides
Lipid Peroxidation
Animals
Lipids
Thiobarbituric Acid Reactive Substances
DNA
Neurology
Biomarkers
Cytochromes c
1,4-dioxin
Polychlorinated Dibenzodioxins
Central Nervous System
Liver

All Science Journal Classification (ASJC) codes

  • Toxicology

Cite this

Induction of oxidative stress in brain tissues of mice after subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. / Hassoun, Ezdihar A.; Wilt, Shawn C.; Devito, Michael J.; Van Birgelen, Angelique; Alsharif, Naser Z.; Birnbaum, Linda S.; Stohs, Sidney J.

In: Toxicological Sciences, Vol. 42, No. 1, 03.1998, p. 23-27.

Research output: Contribution to journalArticle

Hassoun, Ezdihar A. ; Wilt, Shawn C. ; Devito, Michael J. ; Van Birgelen, Angelique ; Alsharif, Naser Z. ; Birnbaum, Linda S. ; Stohs, Sidney J. / Induction of oxidative stress in brain tissues of mice after subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin. In: Toxicological Sciences. 1998 ; Vol. 42, No. 1. pp. 23-27.
@article{9c277f3a9e7749b8ad982936ba7021e6,
title = "Induction of oxidative stress in brain tissues of mice after subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin",
abstract = "The ability of single doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to induce oxidative stress in hepatic and some extrahepatic tissues of animals is well documented. However, no previous study has examined the ability of TCDD to induce oxidative stress and tissue damage in brain in vivo. In this study the ability of TCDD to induce oxidative stress in brain tissues of mice was studied after subchronic exposures. Groups of female B6C3F1 mice were treated orally with TCDD (0, 0.45, 1.5, 15, and 150 ng/kg/day) for 13 weeks, 5 days/week. The animals were euthanized 3 days after the last treatment and brain tissues were collected. Biomarkers of oxidative stress including production of superoxide anion, lipid peroxidation, and DNA-single-strand breaks (SSB) were determined. TCDD treatment resulted in significant and dose-dependent increases in the production of superoxide anion as assessed by reduction of cytochrome c. Significant increases were also observed in lipid peroxidation and DNA-SSB in those tissues, as assessed by the presence of thiobarbituric acid-reactive substances and the alkaline elution technique, respectively. These results clearly indicate that subchronic exposure to low doses of TCDD can induce oxidative tissue damage in brain tissues which may at least in part play a role in the effects of TCDD on the central nervous system.",
author = "Hassoun, {Ezdihar A.} and Wilt, {Shawn C.} and Devito, {Michael J.} and {Van Birgelen}, Angelique and Alsharif, {Naser Z.} and Birnbaum, {Linda S.} and Stohs, {Sidney J.}",
year = "1998",
month = "3",
doi = "10.1006/toxs.1997.2411",
language = "English",
volume = "42",
pages = "23--27",
journal = "Toxicological Sciences",
issn = "1096-6080",
publisher = "Oxford University Press",
number = "1",

}

TY - JOUR

T1 - Induction of oxidative stress in brain tissues of mice after subchronic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin

AU - Hassoun, Ezdihar A.

AU - Wilt, Shawn C.

AU - Devito, Michael J.

AU - Van Birgelen, Angelique

AU - Alsharif, Naser Z.

AU - Birnbaum, Linda S.

AU - Stohs, Sidney J.

PY - 1998/3

Y1 - 1998/3

N2 - The ability of single doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to induce oxidative stress in hepatic and some extrahepatic tissues of animals is well documented. However, no previous study has examined the ability of TCDD to induce oxidative stress and tissue damage in brain in vivo. In this study the ability of TCDD to induce oxidative stress in brain tissues of mice was studied after subchronic exposures. Groups of female B6C3F1 mice were treated orally with TCDD (0, 0.45, 1.5, 15, and 150 ng/kg/day) for 13 weeks, 5 days/week. The animals were euthanized 3 days after the last treatment and brain tissues were collected. Biomarkers of oxidative stress including production of superoxide anion, lipid peroxidation, and DNA-single-strand breaks (SSB) were determined. TCDD treatment resulted in significant and dose-dependent increases in the production of superoxide anion as assessed by reduction of cytochrome c. Significant increases were also observed in lipid peroxidation and DNA-SSB in those tissues, as assessed by the presence of thiobarbituric acid-reactive substances and the alkaline elution technique, respectively. These results clearly indicate that subchronic exposure to low doses of TCDD can induce oxidative tissue damage in brain tissues which may at least in part play a role in the effects of TCDD on the central nervous system.

AB - The ability of single doses of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) to induce oxidative stress in hepatic and some extrahepatic tissues of animals is well documented. However, no previous study has examined the ability of TCDD to induce oxidative stress and tissue damage in brain in vivo. In this study the ability of TCDD to induce oxidative stress in brain tissues of mice was studied after subchronic exposures. Groups of female B6C3F1 mice were treated orally with TCDD (0, 0.45, 1.5, 15, and 150 ng/kg/day) for 13 weeks, 5 days/week. The animals were euthanized 3 days after the last treatment and brain tissues were collected. Biomarkers of oxidative stress including production of superoxide anion, lipid peroxidation, and DNA-single-strand breaks (SSB) were determined. TCDD treatment resulted in significant and dose-dependent increases in the production of superoxide anion as assessed by reduction of cytochrome c. Significant increases were also observed in lipid peroxidation and DNA-SSB in those tissues, as assessed by the presence of thiobarbituric acid-reactive substances and the alkaline elution technique, respectively. These results clearly indicate that subchronic exposure to low doses of TCDD can induce oxidative tissue damage in brain tissues which may at least in part play a role in the effects of TCDD on the central nervous system.

UR - http://www.scopus.com/inward/record.url?scp=0031943470&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0031943470&partnerID=8YFLogxK

U2 - 10.1006/toxs.1997.2411

DO - 10.1006/toxs.1997.2411

M3 - Article

VL - 42

SP - 23

EP - 27

JO - Toxicological Sciences

JF - Toxicological Sciences

SN - 1096-6080

IS - 1

ER -