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S Mitjavila

Publications and source records attributed to S Mitjavila.

At least 19 recordsLinked to original sources
PubMed2000

Paraquat and iron-dependent lipid peroxidation. NADPH versus NADPH-generating systems.

The aim of this work was to study the effect of paraquat (P2+) on NADPH iron-dependent lipid peroxidation (basal peroxidation) either in the presence of NADPH or in the presence of NADPH-generating systems. When NADPH is present, P2+ potentiates NADPH iron-dependent lipid peroxidation, but use of NADPH-generating systems cancels this effect. This may be attributed to certain components in NADPH-generating systems such as glucose-6-phosphate and sodium isocitrate, which act as iron chelators. The binding of iron by these molecules facilitates its reduction and enhances its reactivity toward dioxygen molecules, leading to the formation of reactive species capable of initiating lipid peroxidation, such as Fe3+-O2-*. Under these conditions of rapid basal peroxidation, any additional reduction of iron(III) by a reduced form of P2+ (P+*) has no apparent effect on the peroxidation itself, probably because the initial reaction between iron(II) and O2 followed by initiation of the peroxidation are both rate-limiting steps in the process. Consequently, any alteration of the composition of the reacting mixture (e.g., buffers or the generating system) must be taken into consideration because the formation of new iron chelates can change the rate of basal peroxidation and will modify the effect of redoxcycling molecules.

Animals↗
PubMed1997

Potentiation of iron-induced lipid peroxidation by a series of bipyridyls in relation to their ability to reduce iron.

We determine the relative abilities of three bipyridyls (Paraquat P + +, Benzylviologen B + + and Diquat D + +) to stimulate iron-induced lipid peroxidation in relation to their ability to redox cycle and to reduce iron. The ability to redox cycle increases with the redox potential, in the order: P + + < B + + < D + +. The initial rates of Fe3+ reduction increased from P + + to D + + and B + +. NADPH-dependent microsomal lipid peroxidation was measured in different conditions (1) increasing incubation time, 100 microM bipyridyl, 10 microM FeCl3; (2) increasing concentrations of bipyridyls, 10 microM FeCl3, 10 min incubation time; (3) increasing concentrations of FeCl3, 100 microM bipyridyl, 10 min incubation time. Bipyridyls potentiated the production of malondialdehyde (MDA), particularly with the shortest incubation times and the lowest concentrations of FeCl3, in the order of activity P + + < D + + < B + +. The strong correlation between the initial rate of lipid peroxidation and Fe3+ reduction indicates that the rate of Fe3+ reduction determines the intensity of the potentiation effect of bipyridyls on lipid peroxidation--on the condition that the amount of peroxidizable substrate is not the limiting factor.

Animals↗
PubMed1996

Plasma and hepatic antioxidant control and vitamin A nutritional status.

Twenty-seven rats were divided into three groups and fed on diets containing 0.3, 6 or 60 RE (retinol equivalent) retinyl palmitate/g food. After 7 weeks, hepatic vitamin A uptake was found to be more efficient in vitamin A-deficient rats than in rats given adequate vitamin A. We showed that during the metabolic adaptation of the animals to the level of vitamin A in the diet, extensive modifications occur in the antioxidant defences of the organism. In parallel with the increase in the level of vitamin A, the decrease in the level of alpha-tocopherol in the plasma can bring about a greater susceptibility of the lipoproteins to oxidative stress. Similarly, the decrease in the hepatic alpha-tocopherol level and in glutathione peroxidase activity leads to the weakening of the liver's antioxidant defences.

Animals↗
PubMed1995

Dietary lipid and iron status modulate lipid peroxidation in rats with induced adjuvant arthritis.

We studied the effect of dietary lipids on iron metabolism and lipid peroxidation during induced adjuvant arthritis and/or iron overload in rats. We compared a control diet containing corn oil and rapeseed oil with a diet devoid of polyunsaturated fatty acids containing only tripalmitin as lipids. Four subgroups of rats were used with each diet: without further treatment, with induction of adjuvant arthritis, with iron overload, and with induction of adjuvant arthritis and iron overload. The profile of fatty acids present in plasma and in microsomes changed in rats fed the tripalmitin diet. The level of tetra- and pentaunsaturated fatty acids was reduced, and the level of monounsaturated fatty acids and iron stores was increased with respect to control rats. Thus, ingestion of a tripalmitin diet reduced the substrate for lipid peroxidation, as shown by the decrease in thiobarbituric acid-reactive substances in plasma and conjugated dienes in hepatic microsomal fraction. Adjuvant arthritis and iron overload had a synergistic effect on lipid peroxidation and iron storage in liver. Further, in the hepatic microsomal fraction, tripalmitin reduced the levels of cytochrome P-450, and arthritis reduced the levels of cytochrome P-450 and Ca2+ sequestration. Our results suggest that rats fed tripalmitin showed a reduction of lipid peroxidation induced by inflammation or by iron overload, because of the lack of polyunsaturated fatty acids in the diet, although tripalmitin usually increases the iron stores in the body and causes hepatic alterations.

Animals↗
PubMed1995

[Proton magnetic resonance of plasma in the evaluation of systemic effects of cutaneous inflammation in rats].

NMR evaluation of skin rat inflammation, 24 h after UVB exposition and 48 h after vesicatory (croton oil) application, shows significant variations of relaxation times. Cutaneous T1 and T2 are enhanced in both cases, and plasmatic T2 is increased in croton oil inflammation. At the same time, these two inflammations induce in plasma: a significant increase in ceruloplasmin (respectively 70 and 42%); a decrease in iron transferrin (48 and 53%) and iron saturation (%) of transferrin (53 and 68%); an increase in the protein level of 45% for croton oil treated animals. In skin, for each inflammation, T1 is significantly correlated with cutaneous water content (r = 0.6 and r = 0.35). T1 appears to be more representative than T2 of hydration and molecular dynamic modifications, induce by oedema formation. In plasma, T2 is significantly correlated with ceruloplasmin (4 = 0.67) and protein level (r = 0.45), and reflects more specially than T1 the modifications of the medium composition. The decrease in T2 may be the expression of the diminution of the medium water molecules' mobility, in connection with the increase in protein concentration.

Animals↗
PubMed1993

Ca-efflux, from direct membrane injury by CCl4, is elicited by amphiphilic vehicles in vitro.

Direct membrane injury by CCl4, in situations excluding metabolic activation, was evaluated in saponin-permeabilized hepatocytes and in microsomes by measuring immediate Ca2+ efflux. A good correlation appears between the Ca2+ efflux and the level of CCl4 in the membrane and also the variations in fluidity. Mixtures of CCl4 with water-soluble vehicles were used to improve the dispersion of CCl4 in the medium. The mixtures varied in their ability to elicit the membrane effects of CCl4. The performance of ethanol and, to a lesser degree, other alcohols, suggests the existence of a water stable structural organization between CCl4 and these amphiphilic vehicles, facilitating the transfer of CCl4 to the membrane.

Animals↗
PubMed1993

Antioxidant defenses and its modulation by iron in carrageenan-induced inflammation in rats.

The concentration of endogenous antioxidants has been studied in rats with a carrageenan-induced granuloma. This animal model of inflammation allowed us to study the antioxidant defenses and the oxidative stress in plasma and in the site of inflammation (exudate) and their modulation by the levels of iron in the organism after iron-dextran or desferrioxamine administration. In inflamed rats without supplementary treatment, an interrelation between urate, ascorbate and vitamin E levels has been observed and it appears to be an important mechanism to prevent the depletion of the antioxidants. Further, the sulphydryl groups, caeruloplasmin and retinol also contribute to the defense in this experimental model. Iron overload increases the production of malondialdehyde and decreases some antioxidants such as ascorbic acid and SH groups but, on the other hand, it raises the levels of urate and caeruloplasmin. However, the protective effect of desferrioxamine has not been observed, and in our conditions this may be due to the induced mobilization of iron. Our results show that antioxidants have an important role in the prevention of lipid peroxidation by free radicals produced during inflammatory processes. This protective effect depends on the stage of inflammation.

Animals↗
PubMed1992

Superoxide anion scavenging capacity measured by a polarographic method. Comparison with a colourimetric method.

A polarographic method to assess the scavenging capacity of a molecule for O2-. is proposed. This method is based on the fact that O2-. is not detected by the Clark electrode and that a scavenger competes with spontaneous dismutation of O2-. So, the reduction of O2 into O2-. and the decomposition of H2O2 by catalase, releasing O2, show a biphasic kinetic. Various kinetic parameters can be used to calculate the nmol of O2-. scavenged and also supply data on the reaction mechanisms (oxidation or reduction of O2-.) involved in scavenging. This method presents several other advantages: scavenging capacity can be assayed without added indicators which themselves behave as scavengers (as demonstrated for NBT), the presence of scavengers which interfere with the O2-. generating system (xanthine-xanthine oxidase) does not invalidate the measurements made.

Anions↗
PubMed1991

Carrageenan-induced granuloma and iron status in rats with dietary polyunsaturated fatty acid deficiency.

Sprague-Dawley rats were fed for 4 months on a control diet or a polyunsaturated-fatty-acid (PUFA)-deficient diet. The combined effects of iron overload (Fe dextran) or Fe deficiency (desferrioxamine) on carrageenan-induced granuloma were studied. PUFA deficiency induced changes in Fe metabolism, but no alterations in lipid peroxidation variables were observed. Inflammation implied an increase in lipid peroxidation, Fe storage and caeruloplasmin concentration, together with symptoms of anaemia. PUFA deficiency in inflamed rats gave rise to a lower inflammatory response (granuloma weight and prostaglandin E2 concentration) and ethane exhalation. Fe overload potentiated inflammatory and lipid peroxidation processes, whereas Fe deficiency decreased them.

Animals↗
PubMed1990

Implication of membrane functions in toxicology.

The following are defined: the structural and biochemical characteristics of the membrane constituents involved in the functional activity; the importance of the environment of the proteins in the expression of their activity; and the adaptation possibilities of the membrane's functions to the nutritional distortions or to the action of drugs. The membrane's functions, as a hydrophobic barrier and its essential activities, are analysed in relation to their involvement in toxicology with examples of substances having a great specificity of action. On the other hand, the case of substances impairing, in a non-specific way, the membrane's functional state, very frequently the case in food toxicology, is analysed through the modification of the hydrophobic interaction forces that they induce. Two membranes playing a key role in food toxicology are especially studied: the enterocyte brush border, of which the essential function is absorption and which represents the first barrier to the component brought by food; and the smooth endoplasmic reticulum, which counts among its essential functions the detoxication of xenobiotics and the control of cytoplasmic Ca2+ concentration. The consequences on these functions of a change of the membrane's molecular interaction forces under the in vitro action of a series of substances having different lipophilic power (n-aliphatic alcohols, N-phenyl carbamates, methoxybenzene derivatives) are presented. The consequences of nutritional distortions (ethanol administration or diets deficient in essential fatty acids) on the in vivo adaptation of these membranes under conditions which also modify the membrane interaction forces are also considered.

Animals↗
PubMed1989

Nutrition and biomembranes: additional information concerning the incidence of dietary polyunsaturated fatty acids on membrane organization and biological activity.

One of the important questions in biomembranes now is: Do the essential fatty acids (polyunsaturated fatty acids of the n-6 and n-3 series) play an original structural role in the arrangement of the lipid matrix capable, in particular, of triggering modifications of intrinsic protein activities? Preliminary results from our laboratories are presented in rat and piglet fed standard or essential fatty acid-deficient diets. The relative amounts of 18:2 (n-6) and 20:4 (n-6) in total fatty acids of hepatic microsome or enterocyte brush border membrane phospholipids are closely dependent on the type of diet (a globally decreasing effect with deficiency), whereas no differences were observed with relative amounts of cholesterol, phospholipids, and proteins. This effect of deficiency on membrane fatty acids has to be compared to the decreasing specific activities of microsome NADPH-cytochrome c reductase or aniline hydroxylase (studied in rat), to the increasing order of the structure of both membrane microsome and brush border lipid matrix (studied in both rat and piglet), and to the increasing mobility (or accessibility) of the membrane-protein surface-bonded spin-label (studied in the piglet brush border membrane), suggesting a probably defective protein-lipid fit in the case of deficiency. These results could favor conformational change in the whole membrane structure (i.e. proteins and lipids). The specificity of these effects remains to be assessed.

Animals↗
PubMed1989

Interaction of hexachlorocyclohexane (HCH) and chlorpropham (CIPC) in male rats.

Hexachlorocyclohexane (60.0 mg/kg/d) and chlorpropham (50.0 mg/kg/d) given to male rats daily orally for 30 d caused subtle biochemical lesions. The significant rise in the activity of alkaline phosphatase in liver and serum and of GOT and GPT in liver with substantial weight increase of liver has been suggestive of the initiation of biochemical lesions and adaptation of the organism. Very severe hepatocellular damage is forecasted if the pesticides are given for a prolonged period and in higher concentrations to animals.

Alkaline Phosphatase↗
PubMed1988

Activity of liver microsomal Ca2+-ATPase in relation to perturbation of membrane hydrophobic interactions induced by methoxybenzene derivatives and n-aliphatic alcohols.

Changes in the activity of liver microsomal Ca2+-ATPase were studied in the presence of two series of lipophilic compounds: four flavouring substances derived from methoxybenzene and four n-aliphatic alcohols. With each compound the activity was stimulated at lower concentrations and inhibited at higher concentrations. The linear relationship between equiactive concentrations of the compounds and their partition coefficients showed that the enzyme activity was modulated by perturbation of membrane hydrophobic interactions. Measurements carried out by electron-spin resonance (ESR) showed evidence of a decrease in the membrane order induced by these compounds. However, results obtained with the methoxybenzene derivatives showed that the modification in ATPase activity cannot be directly related to the decrease in membrane order. This decrease did not only reflect perturbation of hydrophobic interactions.

Alcohols↗