Microarray analysis of T-2 toxin-induced liver, placenta and fetal liver lesions in pregnant rats

Sehata, Shinya; Kiyosawa, Naoki; Atsumi, Fusako; Ito, Kazumi; Yamoto, Takashi; Teranishi, Munehiro; Uetsuka, Koji; Nakayama, Hiroyuki; Doi, Kunio

doi:10.1016/j.etp.2005.02.005

Cited by 58 publications

(46 citation statements)

References 28 publications

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“…This modification could be due to several factors, since LPO products were consequences of higher oxygen free radicals (34). These results confirm previous findings that had shown an association between T-2 toxin and increased oxidative stress in experimental animals (35). A study by Letteron et al (36) also showed a correlation between higher LPO and greater hepatic damage in rats and humans.…”

Section: Discussionsupporting

confidence: 82%

Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat

Saoudi¹,

Abdelmouleh²,

Ellouze³

et al. 2009

J. Venom. Anim. Toxins incl. Trop. Dis

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ABSTRACT:This study was undertaken to evaluate the effect of pufferfish (Lagocephalus lagocephalus) meat poisoning on hepatic functions of Wistar rats. For this purpose, groups of rats (Lcr, Lcu+b and Lcu-b) received diet supplemented with 10% of raw or cooked meat, respectively, with or without cooking water of L. lagocephalus while groups Mcr and Mcu+b received diet supplemented with 10% of raw or cooked meat of Liza aurata, which were used as a negative control. In Lcu+b group, ALT, AST and ALP rates (hepatic enzyme markers) decreased after two months of treatment, indicating liver damage. We also observed an increase of 54 and 65% of thiobarbituric acid reactive substances (TBARS) in their livers respectively 48 hours and two months after treatment compared to controls. The catalase (CAT) activity in group Lcu+b decreased (p < 0.05) after two periods of treatment, whereas metallothionein (MT) level significantly increased and decreased, respectively after 48 hours and two months. In fact, in the histological analysis of the livers from Lcu+b treated group, we observed an increase in vacuolisation, necrosis, hepatocytes ballooning and sinusoids dilation. These results indicate that L. lagocephalus meat cooked with water produces hepatotoxicity and oxidative damage.

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Section: Discussionsupporting

confidence: 82%

Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat

Saoudi¹,

Abdelmouleh²,

Ellouze³

et al. 2009

J. Venom. Anim. Toxins incl. Trop. Dis

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show abstract

“…Real-time reverse transcriptasepolymerase chain reaction (RT-PCR) is a widely used technique for quantifying mRNA in biological samples, and the advantage over conventional methods for measuring RNA includes its sensitivity, rapidity, high throughput ability, and dynamic range. There are few reports on gene expression profile using microarrays after T-2 toxin exposure in pregnant rats and analysis of fetal liver, placenta, and brain [15,16]. Results of the Sehata et al [15] microarray study showed changes in expression of genes related to apoptosis, lipid metabolism, drug-metabolizing enzymes, and oxidative stress related genes.…”

Section: Introductionmentioning

confidence: 92%

Oxidative damage and gene expression profile of antioxidant enzymes after T‐2 toxin exposure in mice

Chaudhari

Ravindran

Santhosh

et al. 2009

J Biochem & Molecular Tox

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T-2 toxin is one of the most potent trichothecenes, and on exposure causes severe human and animal diseases. We investigated the dose- and time-dependent effect of T-2 toxin on certain biochemical variables, oxidative damage in terms of antioxidant enzyme activity, and gene expression profile in mice. Mice treated intraperitoneally with either 1 LD50 or 2 LD50 dose (5.61 and 11.22 mg/kg body weight, respectively) of T-2 toxin showed significant alterations in hepatic alanine amino transferase, aspartate amino transferase, and lactate dehydrogenase. Significant changes in hepatic lipid peroxidation, depletion of glutathione (GSH), and expression of heat shock protein-70 indicated oxidative damage. We also evaluated the activity of antioxidant enzymes and compared the gene expression profile by quantitative real-time reverse transcriptase-polymerase chain reaction. Except for glutathione reductase (GR), there was a significant increase in activity of glutathione-S-transferase (GST), glutathione peroxidase (GPx), superoxide dismutase (SOD), and catalase at 1 LD50 dose. At 2 LD50 dose, SOD showed decrease in activity, whereas GST, GPx, and catalase showed significant increase. In contrast, gene expression profile showed downregulation in GR, GPx, GST, and catalase at 1 LD50 dose. At 2 LD50 dose except GSH synthetase, all other genes were downregulated. The results clearly show oxidative stress as one of the mechanisms of T-2 toxin-mediated toxicity.

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“…In a study of the mechanism of action of T-2 toxin on the liver, placenta and fetal liver, it was reported that mechanism of T-2 toxin-induced toxicity in pregnant rats is due to oxidative stress followed by the activation of the mitogen-activated protein kinase (MAPK) pathway, finally inducing apoptosis, and that the c-Jun gene was suggested to play an important role in T-2 toxin-induced apoptosis (Sehata et al, 2005). In the present study, we propose another possible underlying molecular mechanism of T-2 toxin-induced chondrocyte apoptosis via the activation of p53 and the regulation of apoptosis-related proteins.…”

Section: Rt-pcr Detection Of Bax Bcl-xl Bcl-2 P53 Fas and Caspasementioning

confidence: 99%

T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes

Chen

Cao

Chu

et al. 2008

J. Zhejiang Univ. Sci. B

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Abstract:Objective: To investigate the effects of T-2 toxin on expressions of Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 on human chondrocytes. Methods: Human chondrocytes were treated with T-2 toxin (1~20 ng/ml) for 5 d. Fas, p53 and other apoptosis-related proteins such as Bax, Bcl-2, Bcl-xL, caspase-3 were determined by Western blot analysis and their mRNA expressions were determined by reverse transcriptase-polymerase chain reaction (RT-PCR). Results: Increases in Fas, p53 and the pro-apoptotic factor Bax protein and mRNA expressions and a decrease of the anti-apoptotic factor Bcl-xL were observed in a dose-dependent manner after exposures to 1~20 ng/ml T-2 toxin, while the expression of the anti-apoptotic factor Bcl-2 was unchanged. Meanwhile, T-2 toxin could also up-regulate the expressions of both pro-caspase-3 and caspase-3 in a dose-dependent manner. Conclusion: These data suggest a possible underlying molecular mechanism for T-2 toxin to induce the apoptosis signaling pathway in human chondrocytes by regulation of apoptosis-related proteins.

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Microarray analysis of T-2 toxin-induced liver, placenta and fetal liver lesions in pregnant rats

Cited by 58 publications

References 28 publications

Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat

Oxidative stress and hepatotoxicity in rats induced by poisonous pufferfish (Lagocephalus lagocephalus) meat

Oxidative damage and gene expression profile of antioxidant enzymes after T‐2 toxin exposure in mice

T-2 toxin-induced apoptosis involving Fas, p53, Bcl-xL, Bcl-2, Bax and caspase-3 signaling pathways in human chondrocytes

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