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Biomedical subjects

G Barrera

Publications and source records attributed to G Barrera.

At least 37 records · Page 2Linked to original sources
PubMed1996

Protein quality and urea kinetics in prepubertal Chilean schoolboys.

Urea kinetics were measured non-invasively in 12 Chilean schoolboys aged 8-10 years who were receiving one of two diets, either predominantly animal protein or predominantly vegetable protein. Both the diets provided an equivalent level of gross protein, 1.2 g/kg/day. The study diets were given for 10 days to enable adaptation to take place. On the eighth day a single oral dose of 15N15N-urea, 100 mg, was given and the amount of label excreted as 15N15-urea in urine over the subsequent 48 hours was measured. There was little difference in any aspect of urea kinetics between the two diets with urea production (animal, 173 +/- 50 mgN/kg/day; vegetable 179 +/- 53 mgN/kg/day), urea excretion (animal, 86 +/- 19 mgN/kg/day; vegetable, 105 +/- 13 mgN/kg/day), urea nitrogen hydrolysis (animal, 87 +/- 49 mgN/kg/day; vegetable, 74 +/- 42 mgN/kg/day), and the salvaged urea-nitrogen derived from hydrolysis which returned to urea formation (animal, 12 +/- 5 mgN/kg/day; vegetable, 17 +/- 9 mgN/kg/day) all being similar. A very high proportion of the salvage nitrogen derived from urea hydrolysis was maintained within the metabolic pool, about 80%, which was equivalent to 0.4 g protein/kg/day. This is the first time urea kinetics have been measured in children of this age and shows that 57% of the ura produced is excreted in urine on average with about 43% of the urea-nitrogen being salvaged for further metabolic interaction. It is concluded that the vegetable based protein diet taken habitually by Chilean children is metabolically equivalent in terms of urea kinetics to a diet based upon animal protein at this level of intake, but that high rates of salvage of urea nitrogen are found on both diets.

Aging↗
PubMed1995

[Biological quality of a milk substitute for school children based on refined flour subjected to enzymatic hydrolysis].

The biological quality of an experimental milk substitute based on a raw wheat flour subjected to enzymatic hydrolysis in comparison to a control product based on extruded flours and milk protein was studied in 35 < > female school age children. The girls were fed their customary diet during 2 consecutive 14 and 12 day periods, and randomized to the experimental and control products in a double blind crossover fashion. Apparent absorption of protein, energy, calcium and phosphorus was evaluated. Mean nitrogen intake from the experimental product was significantly lower (223 vs 244 mg/Kg/d p<0.0001). Absorbed nitrogen was also lower (187 vs 203 mg&kg/d p<0.0001). Energy intake and excretion were similar with both products; 96 and 95% of intake was absorbed for experimental and control products respectively. The mean calcium intake was significantly lower than the experimental product (39.7 vs 60.2 mg/kg/d p<0.0001). Absorbed calcium from the experimental product was 50% of control (20.7 vs. 39.5 mg/Kg/d p<0.0001). Phosphorus intake was also lower with the experimental product relative to control (22.0 vs 27.8 mg/Kg/d p<0.0001) and absorbed P was 13.1 vs 16.5 mg/Kg/d respectively. Both products were well tolerated. We conclude that the experimental product based on wheat flour does not differ significantly in protein and energy digestibility but calcium and phosphorus absorption and digestibility are significantly lower limiting its use in school feeding programs.

Animals↗
PubMed1994

Inhibition of c-myc expression induced by 4-hydroxynonenal, a product of lipid peroxidation, in the HL-60 human leukemic cell line.

4-Hydroxynonenal is a highly reactive aldehyde, produced by cellular lipid peroxidation, able to inhibit cell proliferation "in vitro" and "in vivo". Its concentration in non proliferating cells ranges up to 1 microM, whereas in the highly undifferentiated tumour cells, it is very low or undetectable. We have now demonstrated that micromolar concentrations of 4-hydroxynonenal inhibit c-myc but not N-ras expression in HL-60 human leukemic cells. This inhibitory effect is observed after an incubation of 1 hour with both 1 and 10 microM aldehyde. Moreover, we report that down-regulation of c-myc expression increases when repeated additions of 1 microM 4-hydroxynonenal are performed, to maintain the cells in presence of aldehyde for 7.5 hours. These results indicate that not only the concentration but also the length of exposure to the aldehyde is important in determining the extent of the c-myc expression inhibition and suggest a role of lipid peroxidation products in the control of gene expression.

Aldehydes↗
PubMed1993

Control of neoplastic cell proliferation and differentiation by restoration of 4-hydroxynonenal physiological concentrations.

Several studies point to the existence of an inverse correlation between cellular lipid peroxidation and both cell proliferation and neoplastic transformation. In anaplastic cell lines products of membrane lipid peroxidation are very low or undetectable. Furthermore numerous results demonstrate effect of lipid peroxidation products on central biochemical pathways and intracellular signalling at physiological concentrations. 4-hydroxynonenal (HNE) is one of the most active products of lipid peroxidation. The restoration of HNE physiological concentrations in neoplastic cells may inhibit cell proliferation and modulate cell re-differentiation. This review try to summarize and critically discuss the effects of physiological concentrations of HNE on normal and neoplastic cell line.

Aldehydes↗
PubMed1992

4-Hydroxynonenal, a product of cellular lipid peroxidation, which modulates c-myc and globin gene expression in K562 erythroleukemic cells.

Several studies point to the existence of an inverse correlation between cellular lipid peroxidation and both cell proliferation and neoplastic transformation. Here, we show that 4-hydroxynonenal (HNE) concentrations close to the level found in normal cells (in the range of 1 and 3 microM) can specifically induce changes in the expression of c-myc and gamma-globin mRNA in K562 cells, without inducing any toxic effects or affecting cell viability. Since we have determined that K562 cells have undetectable levels of endogenous lipid peroxidation, all these effects can be assigned to the exogenous HNE treatment. After a 1-h treatment with 1 microM HNE, c-myc mRNA levels decrease transiently during the first 4 h, rebounding later to higher levels, and normalizing to basal expression after 4 days. Run-on experiments show a transient transcriptional block 20 min after HNE treatment and subsequent posttranscriptional regulation. According to S1 mapping, mRNA changes are exerted on c-myc transcripts initiated from both the principal constitutive start sites (P1 and P2). gamma-Globin mRNA levels concomitantly increase 3- to 4-fold, but no significant changes of housekeeping gene expression are observed. On the basis of these results it appears that the restoration in human erythroleukemic K562 cells of HNE concentrations closer to the level in normal cells can modulate the expression of specific genes.

Aldehydes↗
PubMed1992

Vitamin E dietary supplementation inhibits transforming growth factor beta 1 gene expression in the rat liver.

Overexpression of transforming growth factor beta 1 (TGF beta 1) and increased transcription of pro-collagen type I, are known to represent major events implicated in the development of liver fibrosis under either experimental or clinical conditions. Here we report that long-term dietary vitamin E supplementation in animals undergoing an experimental model of liver fibrosis (induced by chronic treatment of rats with carbon tetrachloride) results in a net inhibition of both hepatic TGF beta 1 and alpha 2 (I) procollagen mRNA levels. Moreover, of striking interest is the observation that vitamin E supplementation per so down-modulates basal levels of TGF beta 1 mRNA in the liver of untreated animals, suggesting that a dietary regimen rich in vitamin E may potentially interfere with both the initiation and progression of the fibrosclerotic processes.

Animals↗
PubMed1992

Sweet lupin protein quality in young men.

The protein quality of Lupinus albus cv Multolupa was evaluated in young adult males using the nitrogen balance technique at graded levels of N intake, and compared with egg protein. Lupin protein was consumed at levels of 0.4, 0.6 and 0.8 g/(kg.d) and egg protein at 0.3, 0.45 and 0.6 g/(kg.d). Each period started with 1 d of consuming a protein-free diet; the next 6 d were used as adaptation and the last 4 d for balance. The levels of protein intake were randomly assigned by a modified Latin square. Energy intake was individually adjusted. Mean apparent N digestibility values of lupin protein were 78.8, 76.1 and 70.2% for the levels of 0.8, 0.6 and 0.4 g protein(kg.d), respectively, and 83.8, 78.3 and 67.1% for egg protein consumed at levels of 0.6, 0.45 and 0.3 g protein/(kg.d), respectively. The N balance results obtained when subjects consumed lupin were 16.4, 0.2 and -15.1 mg N/(kg.d) for protein intakes of 0.8, 0.6 and 0.4 g/(kg.d), respectively. Those obtained for egg consumption were 12.6, -3.6 and -17.1 mg N/(kg.d) for protein intakes of 0.6, 0.45 and 0.3 g/(kg.d), respectively. The linear regressions of intake and absorbed N to retained N for lupin were: N retained = -43.41 + 0.50 N intake and N retained = -36.30 + 0.53 N absorbed. The corresponding regressions for egg were: N retained = -45.0 + 0.65 N intake and N retained = -30.65 + 0.58 N absorbed. The net protein utilization of lupin was 77% that of egg protein.

Adolescent↗
PubMed1991

Induction of differentiation in human HL-60 cells by 4-hydroxynonenal, a product of lipid peroxidation.

4-Hydroxynonenal (HNE) is the major diffusible toxic product generated by lipid peroxidation of cellular membranes. The level of lipid peroxidation and, consequently, the concentration of its products are inversely related to the rate of cell proliferation and directly related to the level of cell differentiation. In the present paper the effects of HNE on the proliferation and differentiation of the HL-60 human promyelocytic cell line have been investigated. Repeated treatment at 45-min intervals with HNE (1 microM) was performed to maintain the cells in the presence of the aldehyde for 7 1/2 or 9 h. The effect of HNE on cell proliferation and differentiation was compared with dimethyl sulfoxide (DMSO)-treated cells. HNE causes a strong inhibition of cell growth without affecting cell viability. Moreover, HL-60 cells acquire the capability to produce chemiluminescence after soluble (phorbol myristate acetate) or corpuscolate (zymosan) stimulation. The phagocytic ability has also been calculated by counting the number of cells that phagocytize opsonized zymosan. Values were 43 and 55% after 10 or 12 HNE treatments, respectively, and 88% in DMSO-treated cells. Myeloperoxidase activity, 5 days after treatment, decreased by 85% in either HNE- or DMSO-treated cells while acid phosphatase activity increased with respect to untreated cells. Results obtained indicate that HNE at concentrations close to those found in the normal tissues can induce inhibition of proliferation and induction of differentiation in the HL-60 cell line.

Aldehydes↗
PubMed1991

Effects of 4-hydroxynonenal, a product of lipid peroxidation, on cell proliferation and ornithine decarboxylase activity.

4-hydroxynonenal (HNE) is one of the major breakdown products of cellular lipid peroxidation. Its effects on proliferation, ornithine decarboxylase (ODC) activity and DNA synthesis have been investigated in leukemic cell lines. The cells were incubated for 1 hour with different aldehyde concentrations, then washed and resuspended in medium with fresh foetal calf serum. HNE concentrations ranging from 10(-5) to 10(-6) M significantly inhibited ODC activity when induced by addition of fresh foetal calf serum both in K562 and HL-60 cells. 3H-Thymidine incorporation in K562 cells was also inhibited from 6 to 12 hours after the treatment. The same HNE concentrations did not inhibit ODC activity when added to cytosol, thus a direct action on the enzyme can be excluded. Moreover, HNE did not affect the half-life of ODC, so that a specific effect on ODC synthesis may be supposed. These data indicate a reduction of proliferative capacity of the cells and are consistent with the possibility that HNE, at concentrations close to those found in normal cells, plays a role in the control of cell proliferation.

Aldehydes↗
PubMed1990

Inhibition of the high affinity Ca2(+)-ATPase activity in rat liver plasma membranes following carbon tetrachloride intoxication.

In vivo administration of CCl4 (2.5 ml/kg, body wt.) to rats results in an early and then progressive inhibition of the high affinity Ca2(+)-ATPase activity in rat liver plasma membranes. The derangement to the Ca2(+)-ATPase seems to be independent on a 'solvent effect' of the agent since the in vitro addition of increasing concentrations of either CCl4 or ethanol to control plasma membranes does not affect the enzymatic activity. By using the technique of vitamin E pretreatment of experimental animals we show that the damage to the Ca2(+)-ATPase seems to follow a two-step kinetics. The early inhibition of the enzyme is not prevented by alpha-tocopherol supplementation and seems then unrelated to lipid peroxidative processes. The same procedure is however able to affort a significant protection against the exacerbation of the damage to the Ca2(+)-ATPase becoming evident late during the course of CCl4 intoxication. The high affinity Ca2(+)-ATPase is affected in vitro by 4-hydroxy-nonenal (HNE), a major end-product of lipid peroxidation interacting with -SH groups. Similar results were obtained after the addition to the incubation medium of sulphydryl reagents. The possible mechanisms involved in Ca2(+)-ATPase inhibition are discussed in relation to the development of CCl4 toxicity and to the role of lipid peroxidative processes.

5'-Nucleotidase↗
PubMed1989

Are the catecholestrogens involved in estrogen-induced striatal dopamine receptor supersensitivity?

The ability of tamoxifen, an antiestrogen agent, to antagonise the striatal dopamine receptor hyperactivity induced in rats by chronic treatment with 17 beta-estradiol and 2-hydroxyestradiol or with two receptor blockers (haloperidol and sulpiride) was compared. It was found that tamoxifen antagonised both the increase in [3H]spiperone binding sites and the stereotyped behaviour induced by apomorphine in animals treated with the two steroids but had no effect in animals receiving the two dopamine blockers. These results run counter to the view that introduction of a catechol group in a steroid molecule is of decisive importance in the induction of striatal dopamine receptor hypersensitivity.

Animals↗
PubMed1989

Energy expenditure in underweight free-living adults: impact of energy supplementation as determined by doubly labeled water and indirect calorimetry.

The effect of energy supplementation was evaluated in six underweight adults under free-living conditions. Customary energy intake (EI) over 4 wk and estimated body composition were defined. Then for 12 wk subjects were fed their customary EI under controlled conditions to assure stable energy reserve. Finally, intake was increased by a mean of 720 kcal/d for 8 wk adjusted to increase body fat from 9 to 18%. Body weight (means +/- SD) increased from 55.2 +/- 3.4 to 57.0 +/- 4.2 kg. Body fat gain was highly variable ranging from 0.6 to 3.8 kg. Energy expenditure (EE) by the factorial and doubly labeled water methods did not change. Fat storage accounted for 66% of the supplemental energy; 237 kcal/d remained unaccounted for. EE by the factorial method, which uses indirect calorimetry or isotopic measurements, were highly correlated (r = 0.8; p less than 0.01). Under the conditions of this study EI does not affect EE. The labeled water method permits the evaluation of energy expenditure in free-living conditions.

Body Composition↗
PubMed1987

Subcellular calmodulin distribution in rat liver after CCl4 poisoning.

Disturbed cellular calcium homeostasis has been observed during CCl4 poisoning, with an increase in calcium content 1 h after administration. Intracellular increase of calcium may be expected to alter membrane/cytosol distribution of calmodulin (CaM). This paper investigates changes in rat liver subcellular CaM distribution 30 min, 1 h and 2 h after CCl4 intoxication. The whole liver value remained unchanged, whereas the nuclear fraction increased and the microsomal and cytosolic fraction decreased. This may suggest that CaM is involved in the several liver cell alterations caused by CCl4 poisoning.

Animals↗
PubMed1987

Nitrogen economy in alcoholic patients without liver disease.

Nitrogen balance was studied in five alcoholic patients during alcohol consumption and after 1 or 2 weeks of abstinence, under metabolic ward conditions. Patients had a history of excessive ethanol intake for five years or more. They were intoxicated and otherwise asymptomatic on admission and had been drinking 150 g or more of ethanol daily, for at least one month. Subjects consumed a diet providing vitamins and minerals exceeding RDA values, 45 kcal/kg of body weight and 0.6 g/kg of proteins (as egg protein), for 33 days. During the first 11 days patients received 200 g of ethanol that were isocalorically substituted later by dietary fat and carbohydrates. The results of this study show that, in alcoholic patients while drinking and after seven days of alcohol withdrawal, nitrogen balance is significantly decreased compared to that performed after two weeks of abstinence. Ethanol metabolic rate was found to be increased, compared to controls. It was lower in four of five patients after the second week of abstinence. These results suggest that alcohol abuse increases protein requirements in chronic alcoholic patients even without histologic liver disease or clinical signs of gastroenterologic disorders.

Adult↗
PubMed1987

Effect of 4-hydroxynonenal on c-myc expression.

The 4-hydroxynonenal aldehyde (HNE), a product of lipid peroxidation with high biological activity, inhibits cancerous growths in vivo and in vitro. The mechanism by which this aldehyde acts is not yet understood. The c-myc oncogene seems to be involved in the regulation of cellular multiplication and transformation. We evaluated the c-myc expression and the RNA, DNA and protein synthesis in K562 cells. These cells were incubated for 1 hour in presence of several aldehyde concentrations (range 5.10(-7) to 10(-4)), then washed and kept for 20 hours in a growth medium until used. HNE inhibited both the nucleic acids and protein synthesis in a dose dependent manner, and c-myc expression was evaluated in the K562 cells after incubation with 10(-4) M or 10(-6) M HNE. HNE inhibited c-myc expression only at the highest dose. These preliminary results may suggest that the inhibition of c-myc expression is related to nucleic acid synthesis inhibition following HNE exposure.

Aldehydes↗