PubMed Health⌕ Search

Biomedical subjects

M Curzio

Publications and source records attributed to M Curzio.

At least 37 records · Page 2Linked to original sources
PubMed1986

Chemotactic activity of the lipid peroxidation product 4-hydroxynonenal and homologous hydroxyalkenals.

The effect of the lipid peroxidation product 4-hydroxynonenal and homologous aldehydes (4-hydroxyoctenal, 4-hydroxyundecenal, 4-hydroxytetradecenal and 4-hydroxypentadecenal) on migration and polarization of rat neutrophils was examined. The most effective aldehydes were 4-hydroxyoctenal and 4-hydroxypentadecenal, which stimulated oriented migration at ED50 = 1.4 X 10(-12) M and 1.3 X 10(-12) M, resp., whereas the other aldehydes had ED50 between 1 X 10(-7) and 6 X 10(-11) M. The peptides fMet-Phe and fMet-Leu-Phe used as positive controls had ED50 values of 4.2 X 10(-7) M and 4.5 X 10(-10) M resp. The 4-hydroxyalkenals induced only a small increase of the percentage of polarized cell and did not enhance the random migration. The effects of 4-hydroxyalkenals were only observed when the incubation buffer contained bovine serum albumin (BSA), in the absence of BSA neither the aldehydes nor the peptides exhibited chemotactic properties. Since the aldehydes easily react with the sulfhydryl groups of the BSA to form the S-alkylated BSA in an equilibrium reaction, the chemotactic substance could either be the free aldehyde or the BSA-aldehyde adduct. The adduct prepared from BSA and 4-hydroxynonenal was chemotactic at doses of 0.65 to 0.0065 mg/ml, when tested in the presence of unmodified BSA. Since the adduct released free 4-hydroxyalkenal during the assay in the reverse reaction, it can not be decided whether the active principle is the aldehyde itself or the aldehyde attached to the BSA. From the effective doses of the aldehydes (10(-7) to 10(-12)M) and the BSA-aldehyde adduct it appears very unlikely that the BSA itself gained chemotactic properties through the alkylation of its sulfhydryl groups by the aldehyde.

Aldehydes↗
PubMed1985

Association of ulcerative colitis, sclerosing cholangitis and cholangiocarcinoma in a patient with IgA deficiency.

A case of an unusual association of ulcerative colitis, sclerosing cholangitis, cholangiocarcinoma and IgA deficiency in a 22-year-old man is reported. The patient was admitted to the hospital with jaundice. Ulcerative colitis had been diagnosed 4 years before. The association of sclerosing cholangitis and cholangiocarcinoma was demonstrated. In addition IgA deficiency was discovered. Possible pathogenetic implications are discussed.

Adenoma, Bile Duct↗
PubMed1985

Chemotactic activity of hydroxyalkenals on rat neutrophils.

Previous results from our laboratory showed that in vitro 4-hydroxyoctenal, 4-hydroxynonenal (HNE) and 4-hydroxytetradecenal elicit a neutrophil chemotactic response in the presence of albumin. Data presented here indicate that other hydroxyalkenals (4-hydroxyundecenal and 4-hydroxy-pentadecenal) also exert a chemotactic attraction on rat pleural neutrophils. The different aldehydes tested show a wide activity-concentration range, the most powerful being 4-hydroxyoctenal. Unlike most chemoattractants, the hydroxyalkenals seem deprived of chemokinetic properties. The mechanism by which these compounds may act on granulocytes is analysed. Experiments investigating the deactivation phenomenon induced by HNE indicate that this aldehyde acts as a chemoattractant by triggering mechanisms different from N-formylmethionyl-leucyl-phenylalanine (fMLP). In fact, cells pre-incubated with this peptide fail to respond chemotactically to the same compound, but are still able to respond to HNE. Similarly, the preventive contact of neutrophils with HNE is unable to influence the chemotactic effect of fMLP.

Aldehydes↗
PubMed1982

[Oriented migration of rat polymorphonucleocytes induced by 4-hydroxynonenal and formylmethionyl-leucyl-phenylalanine].

The influence of the preincubation with 4-hydroxy-2,3-trans-nonenal (HNE) or formylmethionyl-leucyl-phenylalanine (fMLP) on the oriented migration of rat polymorphonuclear leukocytes (PMN) stimulated by fMLP or HNE, respectively, was investigated. Further, the chemotactic effect of the two agents assayed together at doses deprived alone of chemotactic power, was determined. Our results show that the preventive contact of PMN with HNE does not affect the ability of the leukocytes to respond chemotactically to fMLP. Similarly, the cell preincubation with fMLP is unable to influence the HNE chemotactic power. Doses of HNE or fMLP that are not chemotactic alone, stimulate significantly the PMN oriented migration when assayed together.

Aldehydes↗
PubMed1982

Neutrophil chemotactic responses to aldehydes.

The influence of 4-hydroxynonenal (HNE), 4-hydroxytetradecenal (HTDE) and methylglyoxal (MGL) on rat polymorphonuclear leukocyte locomotion has been studied by means of boyden chambers. The two alkenals have been found to exert a chemotactic activity in a range of concentrations between 10-9 and 10-5 M, the most potent chemical being HTDE. The chemotactic effect, however, appeared influenced by the concentration of serum albumin in the medium. In addition, chemotactic doses of the same aldehydes were unable to affect the cell random migration. Higher concentrations of these alkenals depressed both the directed and random locomotion. Methylglyoxal appeared deprived of chemotactic power when assayed at the doses that were active with the above mentioned alkenals and it did not interfere with random migration. 5 X 10-4 M Methylglyoxal exerted a slight, but significant, inhibition of the locomotion events. These results suggest that aldehydes, present at the inflammatory sites, as final products of lipid peroxidation, might play a role in modulating the granulocyte cell locomotion, therefore interfering with the development of phlogosis.

Aldehydes↗
PubMed1981

[Preliminary data on the influence of 4-hydroxyalkenals on the phagocytic activity polymorphonuclear leukocytes in the rat].

The effect of low concentrations of 4-hydroxy-2-trans-pentenal, 4-hydroxy-2-trans-nonenal and 4-hydroxy-2-trans-tetradecenal (4-hydroxyalkenals produced during lipid peroxidation) was evaluated on the phagocytic activity of polymorphonuclear cells obtained from rat peritoneum. Our results show that the above compounds can influence, at different degrees, the endocytic powers, as measured "in vitro", of leukocytes through an inhibition that appears, to some extent, dose-related. Since lipoperoxidative processes can take place at the inflammed area, aldehydes originating from the peroxidative derangement of fatty acids may play a role in interfering with the cellular reactions at the inflammatory site.

Aldehydes↗
PubMed1981

[Chemotaxis and chemokinesis of rat polymorphonuclear leukocytes in response to 4-hydroxy-2-tetradecenal and 4-hydroxy-2-nonenal].

Since a number of experimental evidences suggests that some lipoperoxidation products can affect leukocyte migration "in vitro", we have investigated the chemotactic and chemokinetic properties of two of these products (4-hydroxy-2,3-trans-tetradecenal and 4-hydroxy-2,3-trans-nonenal) using rat neutrophils. The cells were obtained from the pleural cavity after injection of 1.0 ml isologous serum. The granulocytes were suspended in Hanks' plus BSA 2% and the motility determined by means of a modified Boyden chamber. For evaluating the chemotactic properties, the aldehyde were added into the lower compartment, while for detecting the chemokinetic power, the compounds were placed in both the compartments. Our results show that both the chemicals (in a range between nano- and micromolar concentrations) are able to exert -at different degree- a chemotactic activity. In this connection, the more active aldehyde appeared to be the tetradecenal. On the contrary, the same compounds seem uneffective in stimulating the random migration of polymorphonuclear cells.

Aldehydes↗
PubMed1981

[Influence of thyroid states on PGE2 biosynthesis].

Hyperthyroid and hypothyroid states were induced in the rat by daily injection of 3,3',5-triiodothyronine (T3; 33 microgram/100 g b. wt., ip for 6 days) or by thyroparathyroidectomy, respectively. Control animals underwent only a sham operation or received the T3 vehicle. In these experimental conditions the biosynthesis of PGE2-like substance was determined "in vitro" in the fraction obtained after centrifugation at 80,000xg for 60 min of pooled spleens (5). Assays of PGE2 activity were carried out on rat stomach strip preparations according to Vane (8). In a series of additional experiments the influence of thyroid states on the inhibitory activity exerted by Indomethacin, Oxametacine and Phenylbutazone on PGE2 biosynthesis was also evaluated. The results obtained indicate that the hyperthyroidism induces a significant increase of PGE2 production "in vitro" from added arachidonic acid (100% enhancement above the control values) while thyroparathyroidectomy is unable to interfere with such biosynthetic activity. In addition, the inhibitory effect of Indomethacin, Oxametacine and Phenylbutazone on PGE2 production is not affected by hyperthyroid state whereas hypothyroidism significantly limits the action of the mentioned non-steroid anti-inflammatory agents.

Animals↗
PubMed1981

[Lipid peroxidation in the rat liver after acute inflammation induced by carrageenan. I. Influence of non-steroidal anti-inflammatory agents].

Oral administration of Indomethacin (3 mg/Kg) and Phenylbutazone (200 mg/Kg) induces an increase of TBA reacting substances (TBArs) by total liver homogenates, while treatment with Ibuprofen(200 mg/Kg, os) does not affect the susceptibility of liver tissue to lipid peroxidation. The former compounds do not influence the pro-oxidant action of CCl4 (1,0 ml/Kg, os) as evaluated "in vitro", whereas Ibuprofen appears to limit the extension of the TBArs production induced by the halomethane. The acute inflammatory state determined by carrageenan injection in the rat hind paw does not interfere with the peroxidative derangement found "in vitro" neither in the presence or in the absence of the all mentioned chemicals. Carbon tetrachloride (1,0 ml/Kg, os) is able in depressing significantly the rat paw oedema provoked by carrageenan, but does not potentiates the anti-inflammatory action of non-steroid agents.

Animals↗
PubMed1981

[Susceptibility of the liver to lipid peroxidation after treatment with paracetamol].

Intoxication of rats with paracetamol (2.0 g/kg, b. wt.,os) is not followed by peroxidative decomposition of liver microsomal lipids "in vivo" but seems to interfere with ATPase and 5'-Nucleotidase activity in isolated plasmamembranes. Treatment with reduced glutathione, cys=teine and 2. mercaptopropionylglycine results in partial protection against liver injury provoked by the toxin. However, these sulphydryl compounds are not able to prevent the fall of liver GSH content occurring after paracetamol.

Acetaminophen↗
PubMed1981

The influence of experimental hypo- and hyperthyroid states on acute and chronic inflammatory reactions: modified response to non-steroidal anti-inflammatory agents.

Hyperthyroid and hypothyroid states were induced in rats by administration of triiodothyronine or surgical thyroparathyroidectomy. The anti-inflammatory activity of Indomethacin, Oxametacine and Phenylbutazone was evaluated in these animals using paw oedema provoked by carrageenan granulomas induced by cotton pellets and polyarthritis induced by Freund complete adjuvant. Our results indicate that the hyperthyroid state leads to a significant inhibition of the acute inflammatory response to carrageenan, while hypothyroidism has no effect. There was a marked increase in the anti-inflammatory activity of Indomethacin and Phenylbutazone in hyperthyroid rats. By contrast, in thyroparathyroidectomised animals the anti-inflammatory effect of these drugs appeared less than in euthyroid rats. The hyperthyroid state slightly inhibited the development of the cotton pellet-induced granuloma, while hypothyroidism enhanced it. Treatment of hypothyroid animals with the anti-inflammatory drugs resulted in a significant decrease in the size of the granuloma. In the hyperthyroid state, the activity of the compounds appeared similar to that detected in euthyroid rats. Neither hyperthyroidism, nor hypothyroidism affected the inflammatory response to mycobacterial adjuvant, or the effect of anti-inflammatory drugs on the response. These results suggest that thyroid hormones may influence, to various degrees the development of acute inflammation due to carrageenan, and chronic inflammation due to implanted cotton pellets. Our results indicate also that hyper- and hypothyroid states can modify the response of the rat to some non-steroidal anti-inflammatory drugs.

Animals↗
PubMed1980

[Influence of pretreatment with carbon tetrachloride on paracetamol-induced hepatotoxicity].

The influence of preventive treatment with a low dose of carbon tetrachloride on paracetamol-induced hepatotoxicity was evaluated in the rat. The haloalkane was given intraperitoneally (200 microliter/kg) 48 hours prior to paracetamol (PRCT; 2000 mg/kg, os). In parallel groups of rats were treated with CCl4 or PRCT alone. Twelve hours after paracetamol all the animals were killed. Liver damage was determined by evaluating total lipid and triglyceride accumulation in hepatic tissue and the serum activity of alanine-amino transferase (S.GPT). In addition, both the hepatic concentration of reduced glutathione (GSH) and the production "in vitro" of TBA-reacting compounds by liver homogenate were assayed. The results obtained indicate CCl4 "per se" induces a significant triglyceride accumulation but does not influence either the hepatic GSH level or the leakage of GPT into the blood stream. In addition, the haloalkane does not stimulate the production of TBA-reacting substances by hepatic tissue. Paracetamol, alone, produces a slight increase of hepatic triglycerides while induces a significant (+ 108%) enhancement of S.GPT activity. The drug is also able to stimulate the lipid peroxidation "in vitro", whereas provokes a marked decrease of GSH in liver tissue. Combined treatment with the two poisons results in a minor alteration of hepatocyte function as shown by the lack of GPT in serum and by the reduced fall of hepatic GSH as well as by a decreased production of TBA-reacting compounds. In our opinion, CCl4 partially protects against paracetamol-induced liver injury by interacting with enzymes which are responsible for the biotransformation of PRCT to a reactive arylating species that bind to cell molecules.

Acetaminophen↗
PubMed1979

Inhibition of liver protein degradation in vivo by intensive treatment with cycloheximide.

The AA in experiments performed on male rats treated with 0,5 mCi/kg of cycloheximide have observed an inhibition of liver protein degradation and have suggested two mechanism: 1) cycloheximide prevents the acute proteolytic response induced in fibroblast culture by exposure to serum-deficient media and in rat livers after perfusion probably by inhibiting the lysosomal - autophagic system, without modifications in total activity of lysosome proteinases. 2) It may be that protein degradation rate and level of lysosomal proteinases reinterrelated; the latter probably being a factor controlling the overall cell protein turnover rate.

Animals↗
PubMed1978

[Cholangiocarcinoma in a patient with hepatosplenic atrophy subsequent to thorotrast administration (author's transl)].

A case of cholangiocarcinoma observed in a woman of 38 following carotidographic examination with Thorotrast is described: the presence of radioactivity was also demonstrated by gamma spectrometry. The high mean dose absorbed by the liver (estimated at about 3,000 rad) together with the high relative biological effectiveness of the alpha contribution and the time lapse justify the hypothesis that the neoplasia was caused by irradiation.

Adenoma, Bile Duct↗
PubMed1976

Effects of sulphydryl compounds on abnormal red cell pyruvate kinase.

The effect of some sulphydryl compounds on two new variants of red cell pyruvate kinase (ATP: pyruvate phosphotransferase, PK) is reported. In vitro a striking correction has been obtained of both the qualitative and, in one case, the quantitative defect of red cell PK. In vivo, a correction of the qualitative and quantitative abnormalities has been produced in both patients, with clinical improvement of one of them. These findings, together with the unexpected results in respect to the functional properties of PK found in the affected members of the two families studied, suggest that the PK abnormality is not the cause of the haemolytic anaemia, but an epiphenomenon of a primary unknown defect that apparently involves the red cell thiol groups.

Adenosine Triphosphate↗