T-2 Toxin-induced Toxicity in Pregnant Mice and Rats

Doi, Kunio; Ishigami, Noriaki; Sehata, Shinya

doi:10.3390/ijms9112146

Cited by 80 publications

(47 citation statements)

References 66 publications

(70 reference statements)

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“…In animal experiments, placental apoptosis is induced by such things as glucocorticoid (3), lipopolysaccharide [49], T-2 toxin [50], busulfan [51], and some anticancer drugs [52,53]. In a previous study [46], TUNEL-positive cells found in fetal and maternal part of the placenta were counted on gestation day 20 and the number of apoptotic cells in the maternal part was reported to be higher than the ones in the fetal part.…”

Section: Discussionmentioning

confidence: 97%

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Erboğa

Kanter

2015

Biol Trace Elem Res

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In this study, we aimed to show how cadmium (Cd) affects the trophoblast proliferation and differentiation in the placenta and the apoptotic activity in different gestational days and, hence, its effects of placental development with immunohistochemical and TUNEL techniques. Experimental model of our study consisted of placental development of control and Cd groups on 15, 17, 19, and 21th days of the gestation. Female rats in Cd groups were subcutaneously administered a single dose of 0.5 mg Cd/kg/day dissolved in sodium chloride as 2 mL/kg Cd chloride until the day they sacrificed. Embryo and placenta of female rats were separately removed on 15, 17, 19, and 21th days of the gestation in which the placental development takes place and placentas were processed for microscopic examinations. In the placentas of the control group, all layers were observed to be formed on the 15th gestational day and thereafter a continuous growth was monitored. In the Cd group also all layers existed from the 15th gestational day. However, they were smaller in size than control groups. Frequency of proliferating cell nuclear antigen (PCNA)-positive cells was decreased and the number of apoptotic cells was increased in all the gestational days related to Cd. In conclusion, Cd administered during the pregnancy was observed to cause abnormal placental development by disrupting the normal structure of the placenta, inhibiting the proliferation of trophoblast and increasing the number of apoptotic trophoblast cells.

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Section: Discussionmentioning

confidence: 97%

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Erboğa

Kanter

2015

Biol Trace Elem Res

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“…However, on the basis of previous reports (Bensassi et al, 2012;Ma et al, 2012), it is plausible that DON also exerts its toxicity through oxidative stress. Considering the overall mechanism of cytotoxic effects of DON and T-2 toxin, it is presumed that oxidative stress in addition to protein synthesis inhibition (Dänicke, 2006;Doi et al, 2008;Pestka, 2008) in cells is importantly involved.…”

Section: Figmentioning

confidence: 99%

Toxic effects of T-2 toxin and deoxynivalenol on the mitochondrial electron transport system of cardiomyocytes in rats

et al. 2013

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-The in vitro effects of 2 representative mycotoxins, T-2 toxin and deoxynivalenol (DON), of trichothecene group on the electron transport system (ETS) of mitochondria in rat cardiomyocytes were investigated by measuring oxygen consumption rates (OCR). The ATP-linked OCR and the reserve capacity (RC) of the mitochondria ETS were quantified by a "mitochondria stress test" which was estimated by the OCR responses to oligomycin and carbonyl cyanide-p-trifluoromethoxyphenylhydrazone, with an extracellular flux analyzer. The basal OCR was significantly inhibited by the application of T-2 toxin at concentrations of 6 × 10 -1 to 6 × 10 -5 μM and DON at concentrations of 0.78 to 100 μM for 24 hr. The threshold of cardiomyocyte toxicity was estimated to be between 6.0 × 10 -6 and 6.0 × 10 -5 μM for T-2 toxicity on both ATP-linked OCR and RC and between 0.39 and 0.78 μM on ATP-linked OCR or between 1.56 and 3.13 μM on RC for DON. The decrease in OCR of cardiomyocytes exposed to T-2 toxin with a concentration of 6.0 × 10 -3 and 6.0 × 10 -4 μM was significantly inhibited by antioxidants, catalase and vitamin C. In conclusion, the present study demonstrated, through the direct and real-time measurement of respiratory function in mitochondria, that a marked inhibition of mitochondrial ETS function in cardiomyocytes was induced by T-2 toxin and DON and that the mitochondrial dysfunction by T-2 toxin was largely associated with oxidative stress.

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“…Its acute toxicity is higher than in other mycotoxins (Visconti, 1991). During the acute exposure to high doses of T-2 toxin, in animals exhibit "radiomimetic" symptoms, while extremely high doses can cause cardiovascular dysfunction resemble a shock-like syndrome that can result in death (Ueno, 1984;Doi et al, 2008). T-2 toxin induce some alterations in the membrane structure, which consequently stimulates lipid peroxidation.…”

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confidence: 99%

Gastroprotective effects of novel antidotal combination in rats acutely poisoned by T-2 toxin

Jacević¹,

Rеsаnоvić²,

Bočarov-Stančić³

et al. 2010

Acta vet. (Beogr.)

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The purpose of this experiment was to evaluate the antidotal potencies of methylprednisolone (soluble form, Lemod-solu®), nimesulide, N-acetylcysteine (Fluimucil®) and their combinations in rats treated with 1.0 LD50 (0.23 mg/kg) of trichothecene mycotoxin, T-2 toxin. Their antidotal efficacy was investigated by monitoring their effects on general condition, 24-hour-survival, body weight gain, food and water consumption and pathohistological changes in the gut of Wistar rats acutely treated with a single injection of T-2 toxin during a 4-week period. The highest protective index was obtained with methylprednisolone (2.43). Initial loss of body weight (after first 7 days) was found only in T-2 toxin group. During the whole experiment, in poisoned rats protected by methylprednisolone or methylprednisolone and nimesulide, a significant increase (p<0.001) in body weight gain, food and water consumption in comparison with T-2 toxin group was found. At the end of the experiment, N-acetylcysteine, nimesulide and their combination assured higher (p<0.05) weight gain, food and water consumption in comparison with T-2 toxin group. Signs of hemorrhagic diathesis and necrosis of the gut crypt epithelium and lymphoid tissues were found in the T-2 toxin group. Some of these histological alterations were presented in the gut of poisoned rats treated by nimesulide, Nacetylcysteine and their combination. The gut of T-2 toxin rats treated with a combination of methylprednisolone and nimesulide and especially methylprednisolone alone had a histological structure similar to the control group. These results clearly show that methylprednisolone, a well-known anti-inflammatory and immunosuppressive drug, exerts the best antidotal effect against T-2 toxin intoxication in rats

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T-2 Toxin-induced Toxicity in Pregnant Mice and Rats

Cited by 80 publications

References 66 publications

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Effect of Cadmium on Trophoblast Cell Proliferation and Apoptosis in Different Gestation Periods of Rat Placenta

Toxic effects of T-2 toxin and deoxynivalenol on the mitochondrial electron transport system of cardiomyocytes in rats

Gastroprotective effects of novel antidotal combination in rats acutely poisoned by T-2 toxin

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