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Biomedical subjects

G T Saez

Publications and source records attributed to G T Saez.

12 recordsLinked to original sources
PubMed2004

Bioavailability of phenolic compounds from olive oil and oxidative/antioxidant status at postprandial state in healthy humans.

Olive oil phenolic compounds are generally believed to have beneficial antioxidant effects, but little is known about characteristics of their postprandial bioavailability in natural olive oil at real-life doses. The aim of the present study was to determine the concentrations of olive oil phenolic compounds in urine collected over 24 h (24-h urine) after a bolus ingestion of 25 ml of olive oil with different phenolic content, and to demonstrate the effect of this real-life olive oil dose on postprandial levels of blood lipids and oxidative stress biomarkers, as well as to examine the beneficial effects of olive oil phenols. Oral fat loads of 25 ml olive oil with high, moderate, and low phenolic content were administered to 12 healthy male volunteers in a randomized, controlled, crossover trial. Tyrosol and hydroxytyrosol were absorbed in a dose-dependent manner according to the phenolic content of the olive oil administered. The administered dose of 25 ml, which is close to that used daily in Mediterranean countries, did not induce significant postprandial lipemia nor did it promote an increase of in vivo oxidation markers. With regard to plasma antioxidant enzymes, glutathione peroxidase activity decreased postprandially after low phenolic content olive oil ingestion; however this was not observed after intake of moderate and high phenolic content olive oils. The phenolic content of the olive oils administered may account for the protection of the endogenous antioxidant defenses at postprandial state after ingestion of moderate and high phenolic content olive oils.

Adult↗
PubMed2001

Protection by nitric oxide against liver inflammatory injury in animals carrying a nitric oxide synthase-2 transgene.

The effect of pre-existent hepatic NO synthesis on liver injury induced by lipopolysaccharide was studied in animals carrying a nitric oxide synthase-2 (NOS-2) transgene under the control of the phosphoenolpyruvate carboxykinase (PEPCK) promoter. These animals expressed NOS-2 in liver cells under fasting conditions. Lipopolysaccharide-induced liver injury in D-galactosamine-conditioned mice, which enhanced notably the effect of the endotoxin on the liver, was impaired in animals expressing NOS-2. This protection against inflammatory liver damage was dependent on NO synthesis and was caused by an inhibition of nuclear factor kB (NF-kB) activity and an impairment of the synthesis of the proinflammatory cytokines tumor necrosis factor a and interleukin 1b. These data indicate that intrahepatic synthesis of NO protects liver by inhibiting the release of cascades of proinflammatory mediators and suggest a beneficial role for local delivery of NO in the control of liver injury.

Animals↗
PubMed1995

A new polymorphic site in intron 2 of TP53 characterizes LOH in human tumors by PCR-SSCP.

Many human cancers present deletions of the short arm of chromosome 17, which includes the TP53 locus. We detected a new polymorphism in intron 2 of the TP53 gene using PCR-SSCP and used this polymorphic site as a marker to detect loss of heterozygosity in 135 human tumors (73 soft tissue sarcomas, and 48 colorectal and 14 bladder carcinomas). Heterozygosity for this site was 41.5% in this study group and tumor-specific loss of alleles occurred in 43% of informative cases. Allelic losses were more frequently detected at this site than at that in which restriction fragment length polymorphism (RFLP) is located, as detected by the pHp53B probe. It is concluded that this novel approach has several advantages, including detection of a high incidence of informative cases and minimal tissue requirements.

Base Sequence↗
PubMed1994

p53 mutations in human bladder cancer: genotypic versus phenotypic patterns.

The objective of this study was to characterize the pattern of p53 mutations in bladder cancer. The sensitivity and specificity to detect these mutations using clinical material was assessed for the following assays: immunohistochemistry, restriction-fragment-length polymorphism, single-strand-conformation polymorphism, and sequencing. Discrepancies of reported results aimed at the identification of genetic alterations in the p53 gene may be due to differences in methodology, as well as to deficient morphological evaluation of the source of tissue utilized. In order to address these critical issues, we have implemented a novel experimental design that permits analysis by molecular genetics and immunopathology techniques in any given tissue specimen, allowing morphological correlation with genotypic and phenotypic characteristics of the tissue analyzed. Forty-two patients affected with bladder tumors in whom paired normal and tumor tissues were available were used for the present study. Nuclear immunoreactivities were observed in 26 out of 42 bladder tumors analyzed. Abnormal shifts in mobility were noted in 14 of the 42 cases in distinct exons, with one tumor revealing 3 mutations. There was a strong association between p53 nuclear over-expression and 17p LOH, as well as p53 nuclear over-expression and detection of mutations by SSCP and sequencing. According to receiver-operating-curve statistical analysis, the accuracy of detecting p53 mutations by IHC was estimated to be 90.3%. It is our conclusion that, when properly used, this is a highly sensitive and specific method with simple application using clinical material.

Antibodies, Monoclonal↗
PubMed1994

Absence of MDM-2 gene amplification in experimentally induced tumors regardless of p53 status.

To assess the generality of the hypothesis that murine double-minute-2 (MDM-2) gene amplification complements the absence of p53 mutation during tumor development, we analyzed 143 murine tumors induced by a variety of carcinogenic agents in two different mouse strains. Only three of 143 tumors showed p53 genetic alterations and none showed MDM-2 amplification, indicating the existence of alternative pathways that permit tumor cells to bypass p53-MDM-2 control.

Animals↗
PubMed1989

Effect of caffeine on urea biosynthesis and some related processes, ketone bodies, ATP and liver amino acids.

An increase in urea synthesis has been found in rats administered large doses of caffeine. A parallel increase in urea biosynthesis was also found in hepatocytes isolated from caffeine-treated rats, which confirms a greater capacity for urea synthesis induced by caffeine. This increase appeared only after some days of caffeine treatment; during the first days there was no increase in serum urea levels or in in vitro studies of urea synthesis in isolated hepatocytes. However, no appreciable changes were found in either cytosolic or mitochondrial redox states, or in ATP levels in in vivo and in vitro studies. A parallelism was observed between the decreased amino acid levels in caffeine-treated rats and in isolated hepatocytes incubated with different concentrations of caffeine. Several possible mechanisms to explain these findings are considered in the discussion.

Adenosine Triphosphate↗
PubMed1987

Effect of fasting on amino acid metabolism by lactating mammary gland: studies in women and rats.

Concentrations of free amino acids were measured in human milk and arterial blood from lactating women after an overnight fast or after a controlled breakfast. The concentrations of many free amino acids in milk (except L-tyrosine, L-aspartate, L-asparagine, L-glutamate and L-glutamine) were lower after an overnight fast than after breakfast. Similarly, the arterial concentrations of amino acids were lower except for L-asparagine, L-alanine, L-tyrosine and L-phenylalanine. Net uptake of amino acids by the mammary gland of the lactating rat was significantly lower after starvation for 6 or 24 h than in the fed state because the arteriovenous differences of amino acids and the blood flow were significantly lowered. Starvation produced a significant decrease of 2-amino-[1-14C]isobutyric acid uptake by isolated acini from lactating rat. These results show that short-term starvation decreases the amino acid supply and transport in mammary gland as well as the free amino acid concentration in milk.

Amino Acids↗
PubMed1985

Gamma-glutamyl-amino acids as signals for the hormonal regulation of amino acid uptake by the mammary gland of the lactating rat.

The mammary gland is a good model to study the hormonal regulation of amino acid uptake. Danazol, which decreases gonadotrophin release, causes a fall in gamma-glutamyltranspeptidase (GGT) and in amino acid uptake by the gland. Treatment of the rats with estrogens and progesterone partially reverts this effect. Treatment with gonadotrophins completely reverts it. gamma-Glutamyl-amino acids (GAA) increase the uptake of amino acids by the mammary gland in rats previously treated with bromocriptine. We suggest that GAA may act as signals to stimulate amino acid uptake and that the role of GGT may be to generate that signal.

Amino Acids↗
PubMed1983

The effect of cysteine oxidation on isolated hepatocytes.

Isolated hepatocytes incubated with 4mM-cysteine lose reduced glutathione, adenine nucleotides and intracellular enzymes, thus showing extensive membrane damage. The toxic effects of cysteine are enhanced by NH4Cl. Lactate, ethanol and unsaturated fatty acids afford significant protection against cysteine-induced cytoxicity. Addition of catalase to the incubation medium also protected against cysteine toxicity, indicating that H2O2 formed during the oxidation of cysteine is involved in the toxic effects observed. Under anaerobic conditions cysteine did not cause leakage of lactate dehydrogenase from cells, confirming that rapid autoxidation is an essential condition for development of the toxic effects of cysteine.

Adenosine Triphosphate↗
PubMed1983

Equilibration of metabolic CO2 with preformed CO2 and bicarbonate. An unexpected finding.

Entry of metabolic 14CO2 into urea is shown to occur more readily than it equilibrates with the general pool of cellular plus extracellular bicarbonate plus CO2. Since the sites of CO2 production (pyruvate dehydrogenase and oxoglutarate dehydrogenase) and of fixation (carbamoylphosphate synthetase) are intramitochondrial, it is likely that the fixation of CO2 is also more rapid than its equilibration with the cytoplasmic pool of bicarbonate plus CO2. This observation may point to a more general problem concerning the interpretation of isotope data, when compartmentation or proximity of sites of production and utilisation of metabolites may result in the isotope following a preferred pathway.

Alanine↗
PubMed1983

Effects of cysteine and N-acetyl cysteine on GSH content of brain of adult rats.

Intraperitoneal injections of cysteine or N-acetyl cysteine induce a depletion of reduced glutathione (GSH) in rat brain. The doses required to promote GSH depletion are lower than those reported to cause a disseminate neurodegenerative syndrome. Since physiological GSH concentrations are required to maintain cell membranes, we suggest that consideration of the cysteine-induced GSH depletion is important in attempts to understand the mechanism of cysteine-induced cytotoxicity in brain.

Acetylcysteine↗