Search PubMed⌕ Search

Biomedical subjects

C Rojas

Publications and source records attributed to C Rojas.

At least 37 records · Page 2Linked to original sources
PubMed2000

[Jejunal diverticulosis: a cause of infrequent gastrointestinal hemorrhage. Case report].

Jejunal diverticulosis is a very uncommon acquired disease. Clinical manifestations include acute life threatening complication such as perforation, obstruction and bleeding. Jejunal diverticulosis is an extremely rare site of origin of gastrointestinal bleeding, with fewer than seventy cases reported in the literature. We report a 77-year-old patient with a recurrent severe gastrointestinal bleeding manifested by melena and hematochaezia. During the hospitalization the tagged red blood cell scanning was positive for bleeding in the jejunum. At laparotomy, several large-mouthed diverticula at the proximal jejunum were identified. Approximately 30 centimeters of the involved segment was resected with primary end-to-end anastomosis. Postoperative 7 month evolution has been favorable, without any evidence of rebleeding. This report reviews the literature concerning this disease, discusses some diagnostic methods of studying small bowel bleeding and highlights the need to consider this diagnosis in old patients with a gastrointestinal hemorrhage of unknown origin (Rev Méd Chile 2000; 128: 1133-38).

Aged↗
PubMed1998

The rate of free radical production as a determinant of the rate of aging: evidence from the comparative approach.

The relationship of oxidative stress with maximum life span (MLSP) in different vertebrate species is reviewed. In all animal groups the endogenous levels of enzymatic and non-enzymatic antioxidants in tissues negatively correlate with MLSP and the most longevous animals studied in each group, pigeon or man, show the minimum levels of antioxidants. A possible evolutionary reason for this is that longevous animals produce oxygen radicals at a low rate. This has been analysed at the place where more than 90% of oxygen is consumed in the cell, the mitochondria. All available work agrees that, across species, the longer the life span, the lower the rate of mitochondrial oxygen radical production. This is true even in animal groups that do not conform to the rate of living theory of aging, such as birds. Birds have low rates of mitochondrial oxygen radical production, frequently due to a low free radical leak in their respiratory chain. Possibly the low rate of mitochondrial oxygen radical production of longevous species can decrease oxidative damage at targets important for aging (like mitochondrial DNA) that are situated near the places of free radical generation. A low rate of free radical production can contribute to a low aging rate both in animals that conform to the rate of living (metabolic) theory of aging and in animals with exceptional longevities, like birds and primates. Available research indicates there are at least two main characteristics of longevous species: a high rate of DNA repair together with a low rate of free radical production near DNA. Simultaneous consideration of these two characteristics can explain part of the quantitative differences in longevity between animal species.

Aging↗
PubMed1998

Endotoxin increases oxidative injury to proteins in guinea pig liver: protection by dietary vitamin C.

Current information suggests that oxidative damage plays a key role in septic shock induced by endotoxin. This raises the possibility that dietary antioxidant vitamins could protect against endotoxin damage. In this study, the effects of endotoxin administration on protein and lipid oxidative damage and endogenous antioxidants were studied in the liver of guinea pigs previously supplemented with marginal or optimum levels of dietary vitamin C, vitamin E or both. Vitamins C and E inhibited in vitro lipid peroxidation in endotoxin-treated animals. Endotoxin significantly increased oxidative damage to liver proteins in animals receiving low doses of both vitamins, a result described here for the first time. This increase was totally prevented in guinea pigs supplemented with vitamin C alone or in combination with vitamin E, a treatment which strongly increased liver ascorbate. Vitamin C caused small significant increases in superoxide dismutase and glutathione, increased uric acid, and synergically increased alpha-tocopherol levels in vitamin E-supplemented animals treated with endotoxin. The results show that dietary vitamin C protects against endotoxin-induced oxidative damage to proteins in the guinea pig liver. This seems mainly due to a direct protective effect of the increased hepatic ascorbate levels present in vitamin C-supplemented animals.

Animals↗
PubMed1998

[Direct molecular analysis of FMR-1 gene mutation in patients with fragile Xq syndrome and their families].

BACKGROUND: The unequivocal diagnosis of fragile Xq syndrome is based in the direct analysis of the underlying FMR-1 gene mutation, that consists in an increased number of trinucleotide CGG repetitions. AIM: To study families with fragile Xq syndrome, using the Southern technique for the analysis of the mutation. SUBJECTS AND METHODS: Fifteen individuals, pertaining to 6 families with fragile Xq syndrome, were studied. Clinical, cytogenetic and molecular analysis using Southern technique, were done. RESULTS: Five male individuals had a clinically evident syndrome, confirmed by cytogenetic analysis that showed fragility in 10 to 29% of studied cells. One subject with a clinical picture suggesting fragile Xq had a normal cytogenetic study. The other studied subjects were the mothers of the five subjects with the syndrome, that must be carriers, and four brothers. Molecular analysis showed that seven subjects (5 males) had a complete mutation, five (4 females) were carriers of a pre mutation and three (2 males) did not have the mutation. CONCLUSIONS: The Southern technique allows to verify the normal condition of FRAXA locus, identify carriers and to detect complete mutations in fragile Xq syndrome.

Female↗
PubMed1996

Low fatty acid unsaturation protects against lipid peroxidation in liver mitochondria from long-lived species: the pigeon and human case.

Birds have a much higher maximum longevity (MLSP) than mammals of similar metabolic rate. Recent data showed that pigeon mitochondria produce oxygen radicals at a rate much slower than rat mitochondria, in spite of showing similar levels of oxygen consumption (Free Rad. Res., 21 (1994) 317-328). Since oxidative damage from and to mitochondria seems important in relation to aging and longevity, and mitochondrial membranes are situated at the place where oxygen radicals are generated, we studied protein and lipid peroxidation and fatty acid composition of the three main membrane phospholipids of liver mitochondria from rats (MLSP = 4 years) and pigeons (MLSP = 35 years). It was found that pigeon mitochondria show lower levels of fatty acid unsaturation than rat mitochondria in the three lipid fractions, mainly due to a substitution of highly unsaturated fatty acids (20:4 and 22:6) by linoleic acid (18:2), and that these mitochondria are more resistant to lipid peroxidation. Previous research has also obtained exactly the same major difference in fatty acid composition in human mitochondria when compared to those of rat. Thus, present information suggests that the liver mitochondrial membranes of especially long-lived species show both a low level of free radical production and a low degree of fatty acid unsaturation as important constitutive protective traits to slow down aging.

Animals↗
PubMed1996

Effect of dietary vitamin E levels on fatty acid profiles and nonenzymatic lipid peroxidation in the guinea pig liver.

Guinea pigs were fed for five weeks with three diets containing different levels of vitamin E: LOW (but nondeficient, 15 mg of vitamin E/kg diet), MEDIUM (150 mg/kg diet), and HIGH (1,500 mg/kg diet). Dietary vitamin E supplementation did not change oxidative stress indicators in the hydrophilic compartment but increased liver alpha-tocopherol in a dose-dependent way and strongly decreased sensitivity to nonenzymatic in vitro liver lipid peroxidation. This last effect was already observed in group MEDIUM, and no further decrease in in vitro lipid peroxidation occurred from group MEDIUM to group HIGH. The protective effect of vitamin E against in vitro lipid peroxidation was observed even though an optimum dietary concentration of vitamin C for this animal model was present in the three different vitamin E diets. Both HIGH and LOW vitamin E decreased percentage fatty acid unsaturation in all phospholipid fractions from membrane origin in relation to group MEDIUM. The results, together with previous information, show that both vitamin E and vitamin C at intermediate concentrations are needed for optimal protection against lipid peroxidation and loss of fatty acid unsaturation even in normal nonstressful conditions. These protective concentrations are higher than those needed to avoid deficiency syndromes.

Animals↗
PubMed1996

Endotoxin depletes ascorbate in the guinea pig heart. Protective effects of vitamins C and E against oxidative stress.

The effect of acute endotoxin-induced septic shock on myocardium oxidative stress after low or high vitamin C and/or E dietary supplementation was studied in guinea pigs, laboratory animals which, like human, do not have capacity for ascorbate synthesis. Neither the antioxidant enzymes or GSH were modified by endotoxin and vitamin treatments. Vitamin E showed a strong capacity to protect the myocardium against both enzymatic and non-enzymatic lipid peroxidation even in the presence of endotoxin. Vitamin C supplementation increased heart ascorbate whereas endotoxic shock totally depleted the heart ascorbate of vitamin C supplemented animals without changing vitamin E. Endotoxin significantly increased myocardium uric acid, a marker of ischemia induced oxidative stress, in animals fed with low vitamin C levels. This increase was totally prevented in vitamin C supplemented, but not in vitamin E supplemented animals. Strongly depressed levels of plasma vitamin C have been recently described in sepsis in human patients. The results suggest that ascorbate is a primary antioxidant target in the heart of endotoxin treated mammals lacking the capacity to synthesize ascorbate and that ascorbate can have a protective value against endotoxin-induced free radical damage in the myocardium. Implications of these results for the possible preventive role of vitamin C in humans during sepsis are discussed.

Analysis of Variance↗
PubMed1996

Increase in heart glutathione redox ratio and total antioxidant capacity and decrease in lipid peroxidation after vitamin E dietary supplementation in guinea pigs.

Dietary treatment with three diets differing in vitamin E, Low E (15 mg of vitamin E/kg diet), Medium E (150 mg/kg), or High E (1,500 mg/kg), resulted in guinea pigs with low (but nondeficient), intermediate, or high heart alpha-tocopherol concentration. Neither the antioxidant enzymes superoxide dismutase, catalase, glutathione peroxidase, and reductase, nor the nonenzymatic antioxidants, GSH, ascorbate, and uric acid were homeostatically depressed by increases in heart alpha-tocopherol. Protection from both enzymatic (NADPH dependent) and nonenzymatic (ascorbate-Fe2+) lipid peroxidation was strongly increased by vitamin E supplementation from Low to Medium E whereas no additional gain was obtained from the Medium E to the High E group. The GSH/GSSG and GSH/total glutathione ratios increased as a function of the vitamin E dietary concentration closely resembling the shape of the dependence of heart alpha-tocopherol on dietary vitamin E. The results show the capacity of dietary vitamin E to increase the global antioxidant capacity of the heart and to improve the heart redox status in both the lipid and water-soluble compartments. This capacity occurred at levels six times higher than the minimum daily requirement of vitamin E, even in the presence of optimum dietary vitamin C concentrations and basal unstressed conditions. The need for vitamin E dietary supplementation seems specially important in this tissue due to the low constitutive levels of endogenous enzymatic and nonenzymatic antioxidants present of the mammalian heart in comparison with those of other internal organs.

Animals↗
PubMed1996

Vitamin E decreases urine lipid peroxidation products in young healthy human volunteers under normal conditions.

An experimental study on the effects of supplementation with antioxidant vitamins on urine lipid peroxidation products was performed in 21 young healthy men. The subjects ingested placebo, 1 g of vitamin C, or 100 mg of vitamin E per day just after the midday meal during 30 days. Urine samples were obtained 0, 15 and 30 days after the beginning of the study. These samples were analyzed by spectrophotometry or fluorometry after reaction with thiobarbituric acid. Prescan fluorometric studies of the thiobarbituric acid reactive substances in both malondialdehyde standards and urine samples indicated 503 nm and 548 nm as optimum excitation and emission wavelengths. The fluorescence measurements proved to be superior both in terms of selectivity and capacity of detection of antioxidant effects in relation to spectrophotometry. Identical emission peaks were obtained with malondialdehyde standards and urine samples, showing the specificity of the fluorometric method. When measured by fluorometry, the urine of the subjects supplemented with vitamin E showed significantly and progressively smaller lipid peroxidation products as the time of supplementation increased, reaching a 27% decrease at the end of the longitudinal trial. The results indicate the usefulness of the fluorescent measurement of urine thiobarbituric acid reactive substances to easily and rapidly detect variations in whole body oxidative stress in humans. They also show the capacity of safe vitamin E dietary doses to decrease endogenous oxidative stress in healthy humans routinely performing their normal activities.

Adult↗
PubMed1996

[Persistence of the cognitive effects of early stimulation assessed with an animal model].

Human and animal studies have clearly demonstrated the advantageous effects of sensorially enriched rearing environments. Nevertheless, little work has been done concerning the long-lasting persistence of all these behavioral modifications. To undertake this question, a very early enrichment animal model was used. From days 10 to 24 after birth, 28 male albino rats were exposed to a multisensory stimulated environment, while other 28 littermates constituted the control group. At 3 and 6 months old two cognitive abilities were analyzed; the spatial working memory (short term memory) and the latent learning capacity (long term memory). The results evidenced an improved working memory in both 3 and 6 months old rats exposed to the early enriched environment. Moreover, the adult early stimulated group performed as well as younger subjects both on error scores and speed to solve this test. Only in the adult group of rats a superior latent learning capacity of stimulated subjects was evidenced. To conclude, the early enriched environment induced: a) persistent cognitive benefits in the adult rat and b) a more relevant influence on the subsequent behavior of older rather than younger subjects.

Age Factors↗
PubMed1995

Enzyme inhibition during the conversion of squalene to cholesterol.

Two separate enzymatic assays were developed in order to test the selectivity of inhibitors in cholesterol biosynthesis. One assay detects inhibition of delta 5.7-sterol delta 7-reductase, the enzyme involved in the conversion of 7-dehydrocholesterol to cholesterol. Delta 5.7-Sterol delta 7-reductase was inhibited by both RPR 101821, a protonated cyclohexylamine, and BM 15.766, a piperazine derivative, with IC50 values of 1 microM. The second assay detects accumulation of any of five intermediates (squalene oxide, squalene dioxide, lanosterol, desmosterol, and 7-dehydrocholesterol) upon inhibition of enzymes catalyzing reactions in the conversion of squalene to cholesterol. In this assay, inhibition data were most accurate when control assays exhibited a conversion of squalene to cholesterol in the order of 50%. The time required to attain 50% conversion of squalene to cholesterol was 6 h. Given a high inhibitor to substrate concentration ratio and the possible values of Ki, kon, and koff for the reaction between enzymes and inhibitor to form enzyme-inhibitor complexes, it was predicted that in the presence of inhibitors, intermediate accumulation could still be observed after 6 h incubation. The experimental results were in agreement with this prediction.

Animals↗
PubMed1995

Vitamin E protects guinea pig liver from lipid peroxidation without depressing levels of antioxidants.

Oxidative stress is considered a pathogenic factor in many disorders. The capacity of dietary vitamin E to increase global antioxidant capacity and to decrease lipid peroxidation was studied in the guinea pig, an animal that cannot synthesize ascorbate. Male guinea pigs were subjected for 5 weeks to three diets differing in vitamin E content in the presence of optimum levels of vitamin C: group 15 (15 mg vitamin E/kg diet), group 150 (150 mg/kg), and group 1500 (1500 mg/kg). Hepatic vitamin E increased in the three groups in relation to the level of vitamin E in the diet. The increase in vitamin E between groups 15 and 150 was accompanied by a reduction in sensitivity to enzymatic lipid peroxidation. This did not occur between groups 150 and 1500. The different liver vitamin E concentrations did not affect the antioxidant enzymes superoxide dismutase, catalase, GSH-peroxidase and GSH-reductase, nor the non-enzymatic antioxidants vitamin C, GSH and ascorbate. It is concluded that dietary supplementation with vitamin E, at a level 6 times higher than the minimum daily requirement for guinea pigs, increases protection against hepatic lipid peroxidation without depressing endogenous antioxidant defences. Further increases in vitamin E to megadose levels did not provide additional protection from oxidative stress. The results also suggest that optimum levels of both vitamin C and vitamin E, simultaneously needed for protection against oxidative stress, are much higher than the minimum daily requirements.

Animals↗
PubMed1994

Longevity and antioxidant enzymes, non-enzymatic antioxidants and oxidative stress in the vertebrate lung: a comparative study.

It has been proposed that antioxidants can be longevity determinants in animals. However, no comprehensive study has been conducted to try to relate free radicals with maximum life span. This study compares the lung tissue of various vertebrate species--amphibia, mammals and birds--showing very different and well known maximum life spans and life energy potentials. The lung antioxidant enzymes superoxide dismutase, catalase, Se-dependent and non-Se-dependent glutathione peroxidases, and glutathione reductase showed significantly negative correlations with maximum life span. The same was observed for the lung antioxidants, reduced glutathione and ascorbate. It is concluded that a generalized decrease in tissue antioxidant capacity is a characteristic of longevous species. It is suggested that a low rate of free radical recycling (free-radical generation and scavenging) can be an important factor involved in the evolution of high maximum animal longevities. A low free-radical production could be responsible for a low rate of damage at critical sites such as mitochondrial DNA.

Animals↗
PubMed1994

A decrease of free radical production near critical targets as a cause of maximum longevity in animals.

A comprehensive study was performed on the brains of various vertebrate species showing different life energy potentials in order to find out if free radicals are important determinants of species-specific maximum life span. Brain superoxide dismutase, catalase, Se-dependent and independent GSH-peroxidases, GSH-reductase, and ascorbic acid showed significant inverse correlations with maximum longevity, whereas GSH, uric acid, GSSG/GSH, in vitro peroxidation (thiobarbituric acid test), and malondialdehyde (measured by HPLC), did not correlate with maximum life span. Superoxide dismutase, catalase, GSH-peroxidase, GSH and ascorbate results agree with those previously reported in various independent works using different animal species. GSSG/GSH, and true malondialdehyde (HPLC) results are reported for the first time in relation to maximum longevity. The results suggest that longevous species simultaneously show low antioxidant concentrations and low levels of in vivo free radical production (a low free radical turnover) in their tissues. The "free radical production hypothesis of aging" is proposed: a decrease in oxygen radical production per unit of O2 consumption near critical DNA targets (mitochondria or nucleus) increases the maximum life span of extraordinarily long-lived species like birds, primates, and man. Free radical production near these DNA sites would be a main factor responsible for aging in all the species, in those following Pearl's (Rubner's) metabolic rule as well as in those not following it.

Aging↗
PubMed1994

Dietary vitamin C decreases endogenous protein oxidative damage, malondialdehyde, and lipid peroxidation and maintains fatty acid unsaturation in the guinea pig liver.

Guinea pigs were fed during 5 weeks with three different levels of vitamin C in the diet: 33 (marginal deficiency), 660, or 13,200 mg of vitamin C per kg of diet. The group fed 660 mg of vitamin C/kg of diet showed strongly reduced levels of protein carbonyls (46% decrease), malondialdehyde (HPLC; 72% decrease), and in vitro production of TBARS (both stimulated with ascorbate-Fe2+ and with NADPH-ADP-Fe2+; 68% and 71% decrease), increased glutathione reductase activity, and increased vitamin C content (48 times higher) in the liver in relation to the group fed 33 mg/kg. The treatment with 660 mg of vitamin C/kg did not decrease any of the antioxidant defenses studied: superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, GSH, vitamin E, or uric acid. Further supplementation with 13,200 mg vitamin C/kg also reduced protein and lipid peroxidation, but decreased hepatic glutathione reductase and uric acid and resulted in a lower body weight of the animals. Both low (33 mg/kg) and very high (13,200 mg/kg) levels of vitamin C decreased body weight, glutathione reductase, and unsaturation of fatty acids in membrane lipids. The results show that a diet supplying an amount of vitamin C 40 times higher than the minimum daily requirement to avoid scurvy increases the global antioxidant capacity and is of protective value against endogenous lipid and protein oxidation in the liver under normal nonstressful conditions.

Animals↗
PubMed1994

Effect of dietary vitamin C and catalase inhibition of antioxidants and molecular markers of oxidative damage in guinea pigs.

Guinea pigs were fed for five weeks with two diets with different levels of vitamin C, low (33 mg of Vit C/Kg diet) and high (13,200 mg of Vit C/Kg of diet). Catalase was inhibited with 3-amino-1,2,4-triazole (AT) in half of the animals from each dietary group. AT caused an almost complete depletion of liver catalase activity (90%) in both dietary groups. Vitamin C supplementation increased total glutathione peroxidase activity and tissue vitamin C level and decreased levels of protein carbonyls and malondialdehyde (MDA) in both treated and non-treated animals. This vitamin C supplementation did not change any of the other antioxidant defences studied. Our results show that dietary vitamin C supplementation increases global antioxidant capacity and decreases endogenous oxidative damage in the guinea pig liver under normal non-stressful conditions. This supports the protective value of dietary antioxidant supplementation.

Amitrole↗