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Morphologic effects of Vitamin E on hepatic regeneration induced by partial hepatectomy in ethanol exposed rats
S130
Abstracts / Toxicology Letters 164S (2006) S1–S324
The partially protective effect of DMSO against HU induced developmental damage was shown. Therefore, the effect observed could be related to the antioxidant activity of DMSO. HU induced teratogenic insults have been shown to be probably mediated by DNA synthesis inhibition, in addition to oxidative damage. More research is needed to clarify the mechanism involved in DMSO antiteratogenic effects.
P7-03 Effect of adrenaline and oxygen free radicals on calcium tolerant cardiomyocytes: Formation of glutathione adducts Vera Costa 1 , M´arcia Carvalho 2 , F´elix Carvalho 1 , Maria Lourdes Bastos 1 , Rui Carvalho 3 , Fernando Remi˜ao 1 1 Faculdade
doi:10.1016/j.toxlet.2006.06.272 P7-02 Morphologic effects of Vitamin E on hepatic regeneration induced by partial hepatectomy in ethanol exposed rats R. Perez-Pasten 1 , J.A. Morales Gonz´alez 1 , P.R. 2 3 Salda˜na , J.B. Romero , S.R. Mendiola 2 , R.I.S. 2 Dom´ınguez , A.K. Bernardino Gonz´alez 2 1 Pharmacy Academic Area, Health Sciences Institute, Autonomous, University of the State of Hidalgo, Mexico; 2 UNAM; 3 Vicente Guerrero, Hospital-IMSS
The morphological effect of Vitamin E during ethanolinduced hepatic regeneration (HR) inhibition was investigated. Partial hepatectomy (HP) was performed on adult Male Wistar rats. After HP, animals were treated with ethanol alone or ethanol plus Vitamin E at different doses. HP and sham HP rats were used as controls. Ethanol 36% (v/v) was dispensed for 7 days, while Vitamin E was administered daily at the following doses: 100, 200, or 400 international units (IU). At day 7, rat livers were obtained for weight gain determination, in addition to light microscopy analysis. Light microscopy demonstrated that HP induces cellular disorganization and an increase of mitosis. Ethanol provoked an increase in fat droplets, inflammatory infiltrate and congested cells, as well as absence of mitosis. On the contrary, Vitamin E administration reverted ethanol-induced changes, this effect was evident at the 200 and 400 IU. These data demonstrate that Vitamin E possesses a protector effect on ethanol-induced morphologic changes during hepatic regeneration. To ascertain the mechanism of action of Vitamin E additional studies at cellular as well as at molecular levels are needed. doi:10.1016/j.toxlet.2006.06.273
de Farm´acia, Universidade do Porto, 2 Faculdade de, Ciˆ Porto, Portugal; encias da Sa´ude, Universidade Fernando Pessoa, Porto, Portugal; 3 Centro de Neurociˆencias de Coimbra, Coimbra, Portugal Cardiovascular diseases are one of the most common causes of death in the Western World. During the ischemic/reperfusion process in the heart, large amounts of catecholamines are released and reactive oxygen species are generated. Freshly isolated cardiomyocytes have been used as a model for cardiotoxicity studies and previous studies reported that the catecholamine oxidation process was deleterious to these cells. One of the aims of the present work was to establish the effects of catecholamines in the presence or absence of a system capable of generating oxygen free radicals. Superoxide radical was generated using the xanthine (0.1 mM) and xanthine oxidase (0.01 U/mL) system (X/XO). The oxidative stress insult was assessed by evaluating intracellular glutathione levels. Incubation of cardiomyocytes with adrenaline (0.5 mM) for 3 h induced a significative depletion of total and reduced glutathione. While the X/XO system had no observable effect, the concomitant incubation of X/XO and adrenaline resulted in a significant potentiation of adrenaline’s mediated effect on lowering the levels of glutathione. Furthermore, glutathionyladrenaline adduct was found by HPLC with electrochemical detection both in the cells and in the extracellular medium in the suspensions incubated with adrenaline in the presence or absence of superoxide radicals. In spite of this deleterious effect, there was no change in cardiomyocytes viability during the end-points tested. In conclusion, the reactivity of adrenaline, in presence or absence of superoxide, in freshly isolated cardiomyocytes leads to oxidative stress, reflected by the loss of intracellular glutathione homeostasis. The formation of adrenaline adducts with nucleophilic groups, as glutathione, decreases cell’s defence levels, which may ultimately result in cardiotoxicity.
Abstracts / Toxicology Letters 164S (2006) S1–S324
The partially protective effect of DMSO against HU induced developmental damage was shown. Therefore, the effect observed could be related to the antioxidant activity of DMSO. HU induced teratogenic insults have been shown to be probably mediated by DNA synthesis inhibition, in addition to oxidative damage. More research is needed to clarify the mechanism involved in DMSO antiteratogenic effects.
P7-03 Effect of adrenaline and oxygen free radicals on calcium tolerant cardiomyocytes: Formation of glutathione adducts Vera Costa 1 , M´arcia Carvalho 2 , F´elix Carvalho 1 , Maria Lourdes Bastos 1 , Rui Carvalho 3 , Fernando Remi˜ao 1 1 Faculdade
doi:10.1016/j.toxlet.2006.06.272 P7-02 Morphologic effects of Vitamin E on hepatic regeneration induced by partial hepatectomy in ethanol exposed rats R. Perez-Pasten 1 , J.A. Morales Gonz´alez 1 , P.R. 2 3 Salda˜na , J.B. Romero , S.R. Mendiola 2 , R.I.S. 2 Dom´ınguez , A.K. Bernardino Gonz´alez 2 1 Pharmacy Academic Area, Health Sciences Institute, Autonomous, University of the State of Hidalgo, Mexico; 2 UNAM; 3 Vicente Guerrero, Hospital-IMSS
The morphological effect of Vitamin E during ethanolinduced hepatic regeneration (HR) inhibition was investigated. Partial hepatectomy (HP) was performed on adult Male Wistar rats. After HP, animals were treated with ethanol alone or ethanol plus Vitamin E at different doses. HP and sham HP rats were used as controls. Ethanol 36% (v/v) was dispensed for 7 days, while Vitamin E was administered daily at the following doses: 100, 200, or 400 international units (IU). At day 7, rat livers were obtained for weight gain determination, in addition to light microscopy analysis. Light microscopy demonstrated that HP induces cellular disorganization and an increase of mitosis. Ethanol provoked an increase in fat droplets, inflammatory infiltrate and congested cells, as well as absence of mitosis. On the contrary, Vitamin E administration reverted ethanol-induced changes, this effect was evident at the 200 and 400 IU. These data demonstrate that Vitamin E possesses a protector effect on ethanol-induced morphologic changes during hepatic regeneration. To ascertain the mechanism of action of Vitamin E additional studies at cellular as well as at molecular levels are needed. doi:10.1016/j.toxlet.2006.06.273
de Farm´acia, Universidade do Porto, 2 Faculdade de, Ciˆ Porto, Portugal; encias da Sa´ude, Universidade Fernando Pessoa, Porto, Portugal; 3 Centro de Neurociˆencias de Coimbra, Coimbra, Portugal Cardiovascular diseases are one of the most common causes of death in the Western World. During the ischemic/reperfusion process in the heart, large amounts of catecholamines are released and reactive oxygen species are generated. Freshly isolated cardiomyocytes have been used as a model for cardiotoxicity studies and previous studies reported that the catecholamine oxidation process was deleterious to these cells. One of the aims of the present work was to establish the effects of catecholamines in the presence or absence of a system capable of generating oxygen free radicals. Superoxide radical was generated using the xanthine (0.1 mM) and xanthine oxidase (0.01 U/mL) system (X/XO). The oxidative stress insult was assessed by evaluating intracellular glutathione levels. Incubation of cardiomyocytes with adrenaline (0.5 mM) for 3 h induced a significative depletion of total and reduced glutathione. While the X/XO system had no observable effect, the concomitant incubation of X/XO and adrenaline resulted in a significant potentiation of adrenaline’s mediated effect on lowering the levels of glutathione. Furthermore, glutathionyladrenaline adduct was found by HPLC with electrochemical detection both in the cells and in the extracellular medium in the suspensions incubated with adrenaline in the presence or absence of superoxide radicals. In spite of this deleterious effect, there was no change in cardiomyocytes viability during the end-points tested. In conclusion, the reactivity of adrenaline, in presence or absence of superoxide, in freshly isolated cardiomyocytes leads to oxidative stress, reflected by the loss of intracellular glutathione homeostasis. The formation of adrenaline adducts with nucleophilic groups, as glutathione, decreases cell’s defence levels, which may ultimately result in cardiotoxicity.