The relative abilities of TCDD and its congeners to induce oxidative stress in the hepatic and brain tissues of rats after subchronic exposure

Hassoun, Ezdihar A.; Li, Feng; Abushaban, Ahmed; Stohs, Sidney J.

doi:10.1016/s0300-483x(99)00221-8

Cited by 90 publications

(63 citation statements)

References 45 publications

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“…TCDD increases oxidative stress in hepatic and brain tissues of rats (Hassoun et al 2000;Shertzer 2010). …”

Section: Discussionmentioning

confidence: 99%

“…The studies have suggested that these effects are mediated by the aryl hydrocarbon receptor (AhR) and oxidative stress is an important constituent in the mechanism of TCDD toxicity. The exposures of mice and rats to different doses of TCDD have resulted in increases in the production of reactive oxygen species (ROS), lipid peroxidation (LPO), and DNA damage (Hassoun et al 2000;Reyes-Hernánde et al 2010;Aly and Khafagy 2011). Hence, TCDD has been shown to be responsible for multi-site cancers in experimental animals (Bock 1994;Grassman et al 1998).…”

Section: Introductionmentioning

confidence: 99%

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Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

et al. 2011

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2,3,7,8-Tetrachlorodibenzo-p-dioxin (TCDD) is a persistent and ubiquitous environmental contaminant. The health impact of TCDD exposure is of great concern to the general public. Recent reports have implied that eicosapentaenoic acid (EPA) might be a potential chemopreventive agent and influence hepatotoxicity. The aim of the current study was to explore the effectiveness of EPA in alleviating the toxicity of TCDD on primary cultured rat hepatocytes. EPA (5, 10 and 20 lM) was added to cultures alone or simultaneously with TCDD (5 and 10 lM). Rat hepatocytes were treated with TCDD and EPA for 48 h, and then cytotoxicity was detected by [3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide] (MTT) assay and lactate dehydrogenase (LDH) release, while total antioxidant capacity (TAC) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (LMN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD but not EPA decreased cell viability. TCDD also increased TOS level and significantly decreased TAC level in rat hepatocytes in a clear dose dependent manner. On the basis of increasing doses, the dioxin caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG as compared to control culture. Whereas, in cultures treated with EPA alone, TOS level did not change and the level of TAC significantly increased. The presence of EPA with TCDD minimized the toxic effects of the dioxin on primary hepatocytes cultures. Noteworthy, EPA has a protective effect against TCDD-mediated DNA damages.

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“…TCDD increases oxidative stress in hepatic and brain tissues of rats (Hassoun et al 2000;Shertzer 2010). …”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

et al. 2011

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“…With respect to this it should be noted that TCDD and related DLCs are not direct acting genotoxic agents. However they do have the ability to induce oxidative stress and hepatic oxidative DNA damage after prolonged exposure (Hassoun et al, 2000(Hassoun et al, , 2001Wyde et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Olfactory Epithelial Metaplasia and Hyperplasia in Female Harlan Sprague–Dawley Rats Following Chronic Treatment with Polychlorinated Biphenyls

Nyska

Yoshizawa²,

Jokinen

et al. 2005

Toxicol Pathol

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The National Toxicology Program recently completed a series of studies to evaluate the relative potency for toxicity and carcinogenicity of several polyhalogenated aromatic hydrocarbons including dioxin-like compounds (DLCs) and polychlorinated biphenyls. Female Sprague-Dawley rats were administered by gavage for up to 2 years with 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD); 3,3 ,4,4 ,5-pentachlorobiphenyl (PCB126); 2,3,4,7,8-pentachlorodibenzofuran (PeCDF); 2,2 ,4,4 ,5,5 -hexachlorobiphenyl (PCB153); a tertiary mixture of TCDD, PCB126, and PeCDF; a binary mixture of PCB126 and 153; or a binary mixture of PCB126 and 2,3 ,4,4 ,5-pentachlorobiphenyl (PCB118); control animals received corn oil-acetone vehicle (99:1) alone. Nasal epithelial changes were observed only in animals exposed for 2 years to the higher doses of the binary mixtures of PCB126 + PCB153 (1000 ng/kg and 1000 ug/kg) and PCB126 + PCB118 (216 and 360 ng TCDD equivalents/kg). In both studies, the changes were of the same nonneoplastic nature, localized to nasal sections II and III located, respectively, at the level of the incisive papilla anterior to the first palatial ridge (section II) and through the middle of the second molar teeth (section III). The changes consisted of hyperplasia of the respiratory epithelium (level II) and metaplasia of olfactory epithelium to respiratory epithelium with further hyperplasia of the metaplastic respiratory epithelium (levels II and III). Variable amounts of acute inflammatory exudate appeared within the lumen of the nasal cavity, overlying the affected epithelium. Occasionally, the inflammation eroded through the skull and into the adjacent olfactory bulbs.

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“…It has also been observed that the ovoexposure of 2,3,7,8 TCDD caused brain lesions and evoked several developmental issues in chick embryo, which was possibly a classic case of dose and duration dependent neurotoxicity of TCDD [15] . Several studies reported that the chronic exposure of PCBs and TCDD produces oxidative stress by ROS, evokes lipid peroxidation and DNA damage in rat brain tissue [16,17] . It was reported earlier that oxidative stress was associated with apoptotic cell death induced by TCDD in human neuronal cell [18] .…”

Section: Introductionmentioning

confidence: 99%

In Vivo Dose and Duration Dependent Effects of a Dioxin (2,3,7,8 TCDD) on Few Lysosomal Enzymes in Mice Brain

Jigyasi¹,

Kundu²

2013

IOSR-JESTFT

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The relative abilities of TCDD and its congeners to induce oxidative stress in the hepatic and brain tissues of rats after subchronic exposure

Cited by 90 publications

References 45 publications

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

Eicosapentaenoic acid protects against 2,3,7,8-tetrachlorodibenzo-p-dioxin-induced hepatic toxicity in cultured rat hepatocytes

Olfactory Epithelial Metaplasia and Hyperplasia in Female Harlan Sprague–Dawley Rats Following Chronic Treatment with Polychlorinated Biphenyls

In Vivo Dose and Duration Dependent Effects of a Dioxin (2,3,7,8 TCDD) on Few Lysosomal Enzymes in Mice Brain

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