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F Caballero

Publications and source records attributed to F Caballero.

At least 55 records · Page 3Linked to original sources
PubMed1998

beta-Carotene partially prevents the damage induced by 1,4-dimethylaminoazobenzene in mice.

Hepatocarcinogenesis (HC) induced by various carcinogens such as 1,4-dimethylaminoazobenzene (DAB) is a multistep and complex process. The anticancer efficacy of beta-carotene (beta C) was evaluated by estimating some biochemical parameters during the initiation stage of HC. beta C dietary supplementation partially prevented the rise in delta-aminolevulinate synthetase activity. P 450 levels were dramatically enhanced in all groups studied. beta C administration did not overcome catalase inactivation due to DAB treatment; however, superoxide dismutase activity levels showed to be less decreased in the DAB + beta C animals in comparison to the DAB group. The great enhancement provoked by DAB of glutathione S-transferase, a proposed marker of HC, was partially reversed by beta C. In conclusion, heme pathway regulation, drug metabolism, and natural oxidative defence systems, strikingly modified in DAB fed animals, were partially controlled by provitamin A. The potential use of beta C in preventing carcinogenesis is suggested.

Animals↗
PubMed1998

Hepatic enzymatic metabolism alterations and oxidative stress during the onset of carcinogenesis: protective role of alpha-tocopherol.

Oxidants play a role in several stages of carcinogenesis. A high antioxidant capacity is expected to protect 'initiated' cells from excessive oxidant toxicity. The aim of this study was to determine the chemopreventive effect of a-tocopherol (alpha-T) on the hepatocarcinogenesis induced with p-dimethylaminoazobenzene (DAB) in mice. The dietary administration of alpha-T completely reversed the induction of delta-aminolevulinate synthetase and glutathione-S-transferase (the tumoral marker enzyme). alpha-T greatly enhanced P 450 levels, which were even higher in animals exposed to DAB. Indirect evidence for the involvement of oxygen radicals in the DAB model of hepatocarcinogenesis was provided by increased levels of thiobarbituric acid reactive species, which were detected in animals with severe liver damage and were assessed by histological analysis. alpha-T reduced the degree of hepatic injury, although this vitamin produced only slight changes in the oxidative parameters evaluated. The use of alpha-T as a potential chemopreventive agent, particularly during the initiation stage of carcinogenesis provoked by DAB, is worthy of further study.

5-Aminolevulinate Synthetase↗
PubMed1997

Successful transplantation of organs retrieved from donors with bacterial meningitis.

BACKGROUND: The shortage of organs for transplantation is the most important factor limiting the number of transplants performed. Consequently, in recent years, criteria for considering a patient as a potential organ donor have been broadened. METHODS: From 1995 through 1996, we have retrieved organs from five donors who were brain dead because of bacterial meningitis. The causative microorganisms were Neisseria meningitidis in one patient, Streptococcus pneumoniae in three patients, and Escherichia coli in one patient. Fifteen organs were retrieved and transplanted into 16 recipients. All the donors and recipients received adequate antibiotic therapy. RESULTS: None of the recipients developed infectious complications caused by the meningeal pathogens. After a follow-up ranging from 4 to 30 months, 12 patients are alive with functioning grafts. The cause of death was noninfectious in the four patients who died. CONCLUSIONS: Our study demonstrates that patients with brain death caused by bacterial meningitis due to meningococci, pneumococci, or E coli may be suitable organ donors. Transplantation of organs from such donors does not increase the risk of infection transmission to the recipient, provided that both donor and recipient had received adequate antibiotic therapy.

Adolescent↗
PubMed1997

Mite-contaminated foods as a cause of anaphylaxis.

BACKGROUND: Although insect and arthropod contamination of certain foods has been recognized for many years, allergic manifestations caused by ingestion of mite allergens have only rarely been reported. OBJECTIVE: The purpose of this study is to present clinical observations in patients who experienced acute anaphylaxis after eating mite-contaminated foods. METHODS: Thirty atopic subjects who were first seen with systemic anaphylaxis precipitated by the ingestion of wheat-containing foods underwent skin prick tests with inhalant and food extracts, as well as with uncontaminated and mite-contaminated wheat flour. Flour samples were examined microscopically for identification and counting of mites. Der p 1 and Der f 1 levels were quantitated by using immunochemical methods. RESULTS: The most common symptoms were breathlessness, angioedema, wheezing, and rhinorrhea, which started between 10 and 240 minutes after eating. Abundant mites were present in the flour obtained from 28 patients; Suidasia spp. mites were found in grated bread from the other two patients. Positive prick test responses to Dermatophagoides farinae-and mite-contaminated flour and negative skin test responses to wheat extract, other food extracts, and uncontaminated wheat flour were found in all patients. Skin test responses were positive in volunteers with mite allergy even after heating the mite-contaminated flour at 100 degrees C. Screening of 35 unselected flour samples demonstrated the presence of mites in 13 of them (37.1%). CONCLUSIONS: Systemic anaphylaxis can occur after the ingestion of heated or unheated mite-contaminated foods. This problem may be more prevalent in tropical and subtropical countries than previously recognized.

Adolescent↗
PubMed1997

Altered heme pathway regulation and drug metabolizing enzyme system in a mouse model of hepatocarcinogenesis: effect of veronal.

1. Male CF 1 mice were fed p-dimethylaminoazobenzene (DAB) for 35 days and received 5,5-diethylbarbituric acid, before or after DAB treatment, with the purpose of investigating whether the onset of the preinitiation stage of carcinogenesis alters the natural regulatory mechanism of the heme pathway. 2. Changes detected in drug metabolizing enzymes are likely to be the consequence of a primary deregulation mechanism of heme metabolism, shown by an increase in delta-aminolevulinic acid synthetase activity and a decrease in microsomal heme oxygenase, which would finally lead to a great enhancement of cytochrome P450 levels. 3. The alterations found here would give rise to a pattern distinctive to that usually observed in the so-called resistant hepatocyte.

5-Aminolevulinate Synthetase↗
PubMed1995

[Changes in the heme metabolic pathway in diabetic patients].

In the last decades several authors have observed a frequent association between diabetes mellitus and porphyria, mainly porphyria cutanea tarda. In previous studies, it has been demonstrated that both d delta d-aminolevulic acid dehydratase (ALA-D) and porphobilinogen deaminase (PBG-D), enzymes of the heme pathway, are inhibited by high concentrations of glucose in vitro in crude preparations of erythrocytes. The activity of these same enzymes was diminished in different tissues obtained from streptozotocin induced diabetic mice. Therefore, we decided to investigate the incidence of heme metabolism alterations in diabetes mellitus in a population of 100 non selected adult patients. The activities of erythrocytic ALA-D and PBG-D were measured. Rhodanese, an enzyme of the sulfocompounds pathway closely related to the regulation of heme biosynthesis, was also studied. Urine porphyrin content as well as the chromatographic pattern of esterified porphyrins were determined. ALA-D and PBG-D activities were diminished in diabetic patients (40% and 20% respectively), while rhodanese was only slightly increased (Fig. 1). ALA-D activity was subnormal in a 92% of the complete diabetic population, while PBG-D activity was less than normal in a 79% of the same population. No significative differences between enzymic activities were observed in the groups insulin and non-insulin dependent (Fig. 3). Urine porphyrin content was increased in 5% of the diabetic population. Chromatographic pattern of urinary porphyrins was notably altered in diabetic patients irrespectively of their porphyrin content (Fig. 4), suggesting an alteration in the enzyme uroporphyrinogen decarboxylase resembling the primary enzymic defect observed in porphyria cutanea tarda.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1992

Heme biosynthesis pathway regulation in a model of hepatocarcinogenesis pre-initiation.

1. Heme regulation before the appearance of hyperplastic nodules was investigated in mice models of hepatocarcinogenesis. 2. With this aim 5-aminolaevulinate synthetase (ALA-S), microsomal heme-oxygenase (MHO), mitochondrial and cytoplasmic rhodanese activities were examined throughout a period of 35 days in animals exposed to dietary p-dimethylaminoazobenzene (DAB). 3. ALA-S activity was significantly diminished (50%) on day 14, then showing a sharply rising profile from day 28 onwards, and reaching 350% on day 35. 4. A similar profile was observed for mitochondrial rhodanese activity. 5. Changes in MHO and cytoplasmic rhodanese activities were almost the opposite to those observed for ALA-S. 6. The distinctive alteration in mitochondrial and cytoplasmic rhodanese would suggest that it plays a subtle role in ALA-S regulation during carcinogenesis initiation through a mechanism that appears to involve subcellular localization controls perhaps by means of the breakage of cystine trisulphide postulated to act as an ALA-S activator. 7. Taking into account the present results, we suggest a probable mechanism for the onset of hepatocarcinogenesis that includes a primary activating liver status, provoking biochemical aberration leading to the stage of initiation of hepatocarcinogenesis involving the whole organ.

5-Aminolevulinate Synthetase↗
PubMed1978

T-cell depletion and in vitro thymosin inducibility in asthmatic children.

Thirty asthmatic children were compared with an equal number of age-matched healthy children. The mean peripheral blood T-lymphocyte level without foetal calf serum was lower in the asthmatic group (mean 970/mm3, as against 1740/mm3; P less than 0.0001), but this difference was abolished by adding foetal calf serum or thymosin, thus explaining how quite severe T-cell deficiency can be missed by widely used methods. The degree of eosinophilia and the degree of elevation of the plasma IgE level in the asthmatic patients were positively correlated. Positive correlations were also shown between the degree of severity of the asthma, the degree of eosinophilia and the degree of elevation of the plasma IgE level, but not the degree of depression of the T-cell numbers. If this T-cell deficiency reflects an inadequate suppression of IgE responses, a clinical trial of thymosin appears to be warranted.

Adolescent↗