Biomedical subjects

E Chiarpotto

Publications and source records attributed to E Chiarpotto.

58 records · Page 4Linked to original sources

PubMed1980

Studies on lipid peroxidation using isolated rat liver cells: the role of singlet oxygen in the propagation of lipid peroxidation ADP-Fe3+ or CCl4 induced.

The separation of lipid peroxidation reactions in two sequential parts, initiation and propagation, has been proposed. Furthermore, it has been shown that some of the propagation reactions following the peroxidative breakdown of membrane lipids may produce singlet oxygen, a highly excited, energetic species of molecular oxygen. To investigate whether singlet oxygen is involved in the propagation of ADP-Fe3+ or CCl4-induced lipid peroxidation, hepatocytes in single cell suspension were treated with the two mentioned drugs in the presence or in the absence of 1,4-diazabicyclo-[2,2,2]octane (DABCO), a known scavenger of singlet oxygen. Only the stimulation of malonaldehyde production due to ADP-Fe3+ was partially prevented by high concentrations of the scavenger, while the CCl4-induced increase of malonaldehyde was not influenced. The results reported here suggest that ADP-iron complex stimulates lipid peroxidation in a way that is somehow different from that occurring in the case of CCl4 poisoning.

Adenosine Diphosphate↗

PubMed1979

Effect of methyl glyoxal on enzyme release and on protein synthesis and secretion by isolated hepatocytes.

The experiments reported in this paper were designed to study some aspects of protein metabolism in isolated rat liver cells treated with methyl glyoxal. Concentrations of this drug not inducing cell damage were able to decrease hepatocyte protein synthesis and secretion. The results obtained using liver cells whose protein was prelabelled suggest that the alpha-ketoaldehyde acts not only through an impairment of protein synthesis but also affecting the secretion pathway itself.

Alanine Transaminase↗

PubMedDate not supplied

4-hydroxynonenal and transforming growth factor-beta1 expression in colon cancer.

In vivo studies on human colon adenocarcinoma showed decreased transforming growth factor-beta1 (TGF-beta1) antiproliferative cytokine content in tumour tissue related to malignancy progression, with a corresponding decrease in lipid peroxidation aldehydic end-product, 4-hydroxynonenal (HNE). The tumour mechanism to escape TGF-beta1-mediated growth inhibition may be due to an altered TGF-beta1 receptor system. Subsequent in vitro analyses showed a differential distribution of TGF-beta1 receptors depending on the human colon cancer cell line considered (CaCo-2 or HT-29): compared to HT-29 cells, CaCo-2 cells showed a decrease of the two main TGF-beta1 receptors, RI and RII. Notwithstanding their partial TGF-beta1 RI and RII deficiency, treatment of CaCo-2 cells with adequate doses of the cytokine (10 ng/ml) was able to induce apoptosis. Of note, co-treatment of these cells with 1 microM HNE increased the apoptotic effect. The constant low concentration of TGF-beta1 in the tumour mass may be related to the low content of antiproliferative HNE observed in colon cancer: the latter phenomenon, which reduces TGF-beta1 production in the tumour area, may represent a favourable condition for neoplastic progression. The enhancement of TGF-beta1-induced apoptosis by HNE in CaCo-2 cells supports this hypothesis. The different transcriptional components regulated by the distinct signaling pathways of these two molecules might be proposed; in particular, crosstalk between the MAPK and the Smad pathway could modulate and co-operate in the transcription of target genes involved in regulation of cell proliferation.

Adenocarcinoma↗

PubMedDate not supplied

Analysis of the carbonyl compounds produced in beta thalassaemic erythrocytes by oxidative stress.

Several carbonyls more toxic than malonaldehyde (MDA) are also generated during the propagation of lipid peroxidation stimulated "in vitro" in human erythrocytes. As regards thalassaemia, after "in vitro" treatment with tert-butyl hydroperoxide (TBHP), the total amount of aldehydes formed (MDA plus the other carbonyls) is significantly increased in the red cells from homozygous as compared to heterozygous and normal subjects. These findings lead to the conclusion that the extent of lipid peroxidation in erythrocytes is actually wider than that measurable in terms of malonaldehyde only, and that aldehydes of the hydroxyalkenal class in particular may play a role in the pathogenesis of reduced red cell survival in haemolytic anaemias.

Aldehydes↗