The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on oxidative enzymes in adipocytes and liver

Kern, Philip A.; Fishman, Renata B.; Song, Wei; Brown, Aliza Dicker; Fonseca, Vivian

doi:10.1016/s0300-483x(01)00564-9

Cited by 57 publications

(43 citation statements)

References 45 publications

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“…The increase in SOD and GR activity may provide a compensatory mechanism for the liver against TCDD-induced oxidative stress. Kern et al (2002) suggested that TCDD increased SOD activity in adipocytes. Our findings are in support with the earlier observations by Senft et al (2002), who reported that dioxin treatment increases GR level in mouse liver mitochondria.…”

Section: Restoration Of Tcdd-induced Antioxidant Changes By Oo Ht Amentioning

confidence: 99%

Olive oil and its phenolic compounds (hydroxytyrosol and tyrosol) ameliorated TCDD-induced heptotoxicity in rats via inhibition of oxidative stress and apoptosis

Kalaiselvan

Muniasamy

Archunan

et al. 2015

Pharmaceutical Biology

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Context: Naturally occurring polyphenols including olive oil (OO) and its constituents hydroxytyrosol (HT) and tyrosol (TY), consumed in the Mediterranean diet, have shown to treat various ailments due to their remarkable antioxidant properties. Objective: The present study investigates the hepatoprotective effects of OO and its phenolic compounds HT and TY against TCDD-induced hepatotoxicity in male Wistar rats. Materials and methods: TCDD was administered at a dose of 100 ng/kg p.o. for 20 d. Administration of OO (10 ml/kg; oral), HT (0.5 mg/kg; oral), and TY (30 mg/kg; i.p) was started 5 d prior to TCDD administration, and continued for 25 d with or without TCDD administration. At the end of the experiment (25 d), blood was taken for biochemical analyses and liver for the measurement of macromolecular damages, antioxidant status, expressions of CYP1A1, and apoptotic factors. Results: TCDD administration resulted in significant (p50.05) increase in the level of hepatic stress markers ALT (101.6 ± 3.07 IU/l), AST (295.0 ± 3.0 IU/l), and ALP (266.66 ± 3.7 IU/l). Also, biochemical analyses of liver reported elevation in nitrite and protein carbonyl content and depletion of NQO1 and HO. However, OO, HT, and TY restored the antioxidant status. Protein expressions by Western Blot technique showed an increase in the level of CYP1A1 and Bax and a decreased level of Bcl-2 on TCDD treatment, and vice versa on OO, HT, and TY treatment. Discussion and conclusion: Our work concludes that dietary supplementation of OO, HT, and TY could serve as a potential preventive drug for TCDD-induced hepatotoxicity.

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Section: Restoration Of Tcdd-induced Antioxidant Changes By Oo Ht Amentioning

confidence: 99%

Olive oil and its phenolic compounds (hydroxytyrosol and tyrosol) ameliorated TCDD-induced heptotoxicity in rats via inhibition of oxidative stress and apoptosis

Kalaiselvan

Muniasamy

Archunan

et al. 2015

Pharmaceutical Biology

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“…Cellular oxidative stress is the result of normal cellular processes and occurs at the level of the mitochondria when proton potential is high (17), when free radicals are generated at the plasma membrane (18), or when cells are exposed to environmental toxins (19). Cellular responses to limit oxidative stress are grouped into phase I and phase II enzymes (20), the latter including heme oxygenase and NAD(P)H:quinone reductase (EC 1.6.99.2).…”

mentioning

confidence: 99%

A Promoter Genotype and Oxidative Stress Potentially Link Resistin to Human Insulin Resistance

et al. 2003

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Insulin resistance is a component of type 2 diabetes and often precedes pancreatic ␤-cell failure. Contributing factors include obesity and a central pattern of fat accumulation with a strong genetic component. The adipocyte secreted hormone resistin has been proposed as a link between the adipocyte and insulin resistance by inhibition of insulin-stimulated glucose uptake and/ or blocking adipocyte differentiation. Here we report that the G/G genotype of a single nucleotide polymorphism (SNP) in the promoter of the human resistin gene, ؊180C>G, had significantly increased basal promoter activity in adipocytes. These data were recapitulated in vivo, where G/G homozygotes had significantly higher resistin mRNA levels in human abdominal subcutaneous fat. A significant interaction was also found between the ؊180C>G SNP, a marker of oxidative stress (NAD[P]H quinone oxidoreductase mRNA) and homeostasis model assessment of insulin resistance. In addition, resistin mRNA was positively and independently correlated with insulin resistance and hepatic fat as measured by liver X-ray attenuation. These data implicate resistin in the pathophysiology of the human insulin resistance syndrome, an effect mediated by the ؊180C>G promoter SNP and potentially cellular oxidative stress.

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“…A hallmark of oxidative stress is lipid peroxidation, which disrupts the structural integrity of cell membranes and can also lead to the formation of aldehydes, which in turn further damage lipids, protein, and DNA. Cells possess defense mechanisms to protect against free radical damage including antioxidant enzymes (superoxide dismutase; SOD, catalase; (CAT) and glutathione peroxidase; GSH-Px) and glutathione which scavenge free radicals to form non-radical products (Kern et al 2002).…”

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

“…In experimental animals, TCDD exposure damaged a number of target organs including liver, thymus, and adipose tissue (Kern et al 2002;Turkez et al 2012a, b). After the administration of TCDD to rodents changes were observed which associated with increased oxidative stress, including increased superoxide formation, lipid peroxidation (Kern et al 2002), and DNA single strand breaks (Shertzer et al 1998). In addition, another study (Slezak et al 2000) demonstrated that indices of oxidative stress were present after both acute and subchronic administration of TCDD to mice, but the ROS production required only low tissue levels of TCDD in the subchronic exposure mice.…”

Section: Introductionmentioning

confidence: 99%

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Ameliorative effect of supplementation with l-glutamine on oxidative stress, DNA damage, cell viability and hepatotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat hepatocyte cultures

et al. 2012

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The most potent of the dioxins, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), is a persistent and ubiquitous environmental contaminant. And the health impact of exposure to TCDD is of great concern to the general public. Recent data indicate that Lglutamine (Gln) has antioxidant properties and may influence hepatotoxicity. The objective of the present study was undertaken to explore the effectiveness of Gln in alleviating the hepatotoxicity of TCDD on primary cultured rat hepatocytes. Gln (0.5, 1 and 2 mM) was added to cultures alone or simultaneously with TCDD (0.005 and 0.01 mM). The hepatocytes were treated with TCDD and Gln for 48 h. Then cell viability 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), total glutathione (TGSH) and total oxidative stress (TOS) levels were determined to evaluate the oxidative injury. The DNA damage was also analyzed by liver micronucleus assay (MN) and 8-oxo-2-deoxyguanosine (8-OH-dG). The results of MTT and LDH assays showed that TCDD decreased cell viability but not L-glutamine. TCDD also increased TOS level in rat hepatocytes and significantly decreased TAC and TGSH levels. On the basis of increasing doses, the dioxin in a dosedependent manner caused significant increases of micronucleated hepatocytes (MNHEPs) and 8-OH-dG as compared to control culture. Whereas, in cultures exposured with Gln alone, TOS levels were not changed and TAC and TGSH together were significantly increased in dose-dependent fashion. The presence of Gln with TCDD modulated the hepatotoxic effects of TCDD on primary hepatocytes cultures. Noteworthy, Gln has a protective effect against TCDD-mediated DNA damages. As conclusion, we reported here an increased potential therapeutic significance of L-glutamine in TCDD-mediated hepatic injury for the first time.

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The effect of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on oxidative enzymes in adipocytes and liver

Cited by 57 publications

References 45 publications

Olive oil and its phenolic compounds (hydroxytyrosol and tyrosol) ameliorated TCDD-induced heptotoxicity in rats via inhibition of oxidative stress and apoptosis

Olive oil and its phenolic compounds (hydroxytyrosol and tyrosol) ameliorated TCDD-induced heptotoxicity in rats via inhibition of oxidative stress and apoptosis

A Promoter Genotype and Oxidative Stress Potentially Link Resistin to Human Insulin Resistance

Ameliorative effect of supplementation with l-glutamine on oxidative stress, DNA damage, cell viability and hepatotoxicity induced by 2,3,7,8-tetrachlorodibenzo-p-dioxin in rat hepatocyte cultures

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