Variations in peroxisomal catalase of neonatal rat hepatocyte subpopulations

Tolosa, D; Azorı́n, Inmaculada; Sancho‐Tello, María; Guerri, Consuelo; Renau‐Piqueras, Jaime

doi:10.1007/bf00203400

Cited by 3 publications

(1 citation statement)

References 57 publications

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“…CAT, a pivotal antioxidant enzyme, can decompose hydrogen peroxide into oxygen and H 2 O. 34 The later results showed that clivorine at the low concentration increased CAT activity weakly, suggesting the possible increase of cellular defensive capacity. The increase of CAT activity also indicates that CAT may play important roles in regulating clivorine-induced toxicity on rat hepatocytes.…”

Section: Discussionmentioning

confidence: 96%

Pyrrolizidine alkaloid clivorine induced oxidative injury on primary cultured rat hepatocytes

Liu

Wang

2010

Hum Exp Toxicol

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Clivorine is an otonecine-type hepatotoxic pyrrolizidine alkaloid (HPAs), to which humans are exposed when consuming herbs containing such components. In the present study, we investigated clivorine-induced oxidative stress injury on primary cultured rat hepatocytes. Rat hepatocytes were treated with various concentrations of clivorine (1—100 μM) for 48 hours, and then cell viability was detected by 3-(4,5-dimethyl-thiazol-2-yl) 2,5-diphenyltetrazolium bromide (MTT) assay, while lipid peroxidation (LPO) level, glutathione peroxidase (GPx), glutathione-S-transferase (GST), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD) activities were determined to evaluate the oxidative injury. The results of MTT assay showed that clivorine decreased cell viability in a concentration-dependent manner. Clivorine also increased LPO amounts in rat hepatocytes at the concentrations of 50 μM and 100 μM. Further results showed that clivorine decreased GPx, GST and GR activities, which are all reduced glutathione (GSH)-related antioxidant enzymes. CAT and SOD are both important antioxidant enzymes, and the results showed that clivorine increased CAT activity at the low concentration of 5 μM and decreased cellular SOD activity at all concentrations. Taken together, our results demonstrated that clivorine induced toxicity on primary cultured rat hepatocytes by causing the damage on cellular redox balance.

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Section: Discussionmentioning

confidence: 96%

Pyrrolizidine alkaloid clivorine induced oxidative injury on primary cultured rat hepatocytes

Liu

Wang

2010

Hum Exp Toxicol

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Prenatal Alcohol Exposure Affects Galactosyltransferase Activity and Glycoconjugates in the Golgi Apparatus of Fetal Rat Hepatocytes

et al. 1997

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been clearly demonstrated in experimental animals, 4,5 in Prenatal exposure to alcohol affects the morphologiwhich important alterations in the ultrastructure of various cal, structural, and functional features of the Golgi appatissues and organs, including the liver, were found to be inratus (GA), thus altering the glycosylation process in feduced by prenatal exposure to ethanol. 6 We have previously tal hepatocytes. To elucidate the cellular mechanisms demonstrated that prenatal exposure to ethanol induces seunderlying these alterations, we have studied the effect vere morphological alterations in newborn rat hepatocytes, of alcohol exposure in utero on the activity of liver galacincluding an increase in the hepatocyte and mitochondrial tosyltransferase, an enzyme involved in the glycosylavolume, 7,8 alterations in the morphology of mitochondria 7,8 tion process, and on the hepatic glycoprotein sugar comand in the characteristics of the lateral plasma membrane of position. For this, livers from 21-day-old fetuses obtained hepatocytes, 9 a decrease in the activities of several phosphafrom control and ethanol-fed rats were used. Galactosyltransferase (GT) activity was determined in isolated GA tases known to be markers of different cell components, 10 and cis and trans fractions. Colloidal gold-labeled lectin cy-increases in the peroxisomal catalase. 11 tochemistry was used to analyze sugar residues in hepaHowever, one of the most striking changes induced by ethatocytes at the subcellular level. Finally, the integrity of nol in the developing hepatocyte is a morphological disorganithe GA after alcohol treatment was assessed by electron zation of the Golgi apparatus (GA), which is accompanied by microscopy and by evaluating the distribution of the alterations in the cytochemical properties of both the cis and Golgi b-COP, a protein involved in vesicular trafficking. trans sides of this organelle, 10,12 suggesting a functional imPrenatal alcohol exposure induces a significant increase pairment of this cell organelle. Indeed, we have shown that in both liver weight and total protein content in the prenatal ethanol exposure to alcohol induces a decrease in trans Golgi. Moreover, this treatment decreases the ac-the synthesis of proteins in the hepatocyte, as well as an tivity of galactosyltransferase, increases a-L-Fuc resi-alteration in the process of glycosylation and/or transport of dues, and reduces the number of a-Man, GlcNAc(b1,4,Gl-secretory glycoproteins, 13 processes that depend on the GA cNAc) 1,2 , GalNAca1,3GalNAc, a-GalNAc, and a-Gal integrity. It is known that the terminal glycosylation of most residues. Alcohol exposure also causes the Golgi cister-secretory proteins occurs in this cell component. The comnae to disappear in about 30% of the hepatocytes, and pleted glycoproteins are then packaged into secretory vesicles reduces 75% the number of anti-Golgi b-COP protein and sorted from the trans-Golgi network to the final destinabinding sites. Our results suggest that the decrease in tions. 14-16 Theref...

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Lead-induced catalase activity differentially modulates behaviors induced by short-chain alcohols

Correa

Pascual

Sanchis‐Segura

et al. 2005

Pharmacology Biochemistry and Behavior

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Variations in peroxisomal catalase of neonatal rat hepatocyte subpopulations

Cited by 3 publications

References 57 publications

Pyrrolizidine alkaloid clivorine induced oxidative injury on primary cultured rat hepatocytes

Pyrrolizidine alkaloid clivorine induced oxidative injury on primary cultured rat hepatocytes

Prenatal Alcohol Exposure Affects Galactosyltransferase Activity and Glycoconjugates in the Golgi Apparatus of Fetal Rat Hepatocytes

Lead-induced catalase activity differentially modulates behaviors induced by short-chain alcohols

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