M L Murillo

Universidad de Sevilla, Hispalis, Andalusia, Spain

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Publications (51)111.19 Total impact

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    ABSTRACT: Purpose: Selenium (Se) has a dual role in metabolic syndrome (MS) development as it has an antioxidant action against both "good" and "bad" reactive oxygen species. This study evaluates Se body profile in dams which present MS during gestation and lactation, in order to elucidate a normal dietary Se's implication in this pathology. Method: Rats were randomized into control (C) and fructose (F) groups. The rich fructose diet (65 %) during gestation and lactation periods induced MS in dams. Se body distribution was determined by atomic absorption spectrophotometry, and the hepatic activity of the four antioxidant enzymes and the bimolecular oxidation were determined by spectrophotometry. The cardiac activity was monitored using the indirect tail occlusion method. Lipid and glucidic profile was also analyzed. Results: Despite the fact that the diet supplied has 0.1 ppm of Se, the minimal dietary requirement for rats, F dams ate less amount of food, and therefore, they had lower Se retention. However, they had normal levels of Se in serum and milk. Dams with MS had Se depletion in heart and muscle joint to hypertension and a lower heart rate, and Se repletion in liver and kidney. Despite the increase in hepatic glutathione peroxidase (GPx) and catalase activity found, lipid oxidation occurred-probably because superoxide dismutase activity was diminished. In heart, the activity and expression of the selenoprotein GPx1 were decreased. Conclusion: With these results, it is not possible to elucidate whether a dietary Se supplementation or a Se-restricted diet are good for MS; because despite the fact that GPx activity is increased in liver, it is also found, for the first time, that heart Se deposits are significantly decreased during MS.
    No preview · Article · Dec 2015 · European Journal of Nutrition
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    M.L. Ojeda · R.M. Rua · F Nogales · J Díaz-Castro · M.L. Murillo · O Carreras
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    ABSTRACT: Aims: An important mechanism in alcohol-induced injury is biomolecular oxidative damage. Folic acid is supplied to chronic alcoholic patients in order to prevent this situation, as this is the main vitamin deficiency that they suffer from. Acute alcohol exposure, such as binge drinking, is one of the most widespread ethanol consumption models practiced by adolescents. However, there is no evidence of folic acid body profiles after this pattern of consumption. Methods: Four groups of adolescent rats were used: control, alcohol (exposed to intraperitoneal binge drinking), control folic acid-supplemented group and alcohol folic acid-supplemented group. Folic acid levels, protein, lipid and DNA oxidative damage in serum, and liver glutathione (GSH) and reduced/oxidized glutathione ratio (GSH/GSSG) were measured. Results: Binge-drinking rats had higher lipids and DNA oxidation levels. They also had lower hepatic GSH levels and GSH/GSSG ratio. Folic acid supplementation to binge-drinking rats does not change the serum protein oxidation but decreases lipid and DNA oxidation. Finally, GSH increased to control levels with folic acid supplementation. Conclusion: Folic acid supplementation is an economic and efficient therapy against the oxidative damage in lipids and mainly in DNA stability caused by binge drinking during adolescence. It has also been demonstrated that folic acid increases GSH levels, improving the antioxidant status and revealing a hepatoprotective effect during binge drinking.
    Full-text · Article · Oct 2015 · Alcohol and Alcoholism
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    ABSTRACT: Antioxidant system abnormalities have been associated with ethanol consumption. This study examines the effects of chronic ethanol consumption on oxidative balance, including selenium (Se) levels in alcoholic patients with or without liver disease, and if these measurements could be indicative of liver disease. Serum Se levels, antioxidant enzymes' activities, malondialdehyde (MDA) and protein carbonyl (PC) were determined in three groups of patients: alcoholics without liver disease, alcoholics with liver disease, and non-alcoholics with liver disease; and in healthy volunteers. Serum Se levels were lower in alcoholic patients and in patients affected by liver disease and especially lower in the alcoholic liver disease group. These values were correlated with the activity of glutathione peroxidase (GPx), the antioxidant selenoprotein. The antioxidant activity of the glutathione reductase (GR) and superoxide dismutase (SOD) were also lower in the three non-healthy groups. However, GR activity decreased and SOD activity increased in the non-alcoholic liver disease group versus alcoholic groups. Higher concentrations of PC in serum were found in non-healthy groups and were higher in alcoholic patients who also showed higher MDA levels. The highest MDA and PC levels were found in the alcoholic liver disease group. We conclude that serum Se levels are drastically decreased in alcoholic liver disease patients, showing this element a direct correlation with GPx activity, and lipid oxidation, suggesting that the serum Se/MDA ratio could be an indicator of hepatic damage caused by alcohol consumption, and pointing out to Se as a possible antioxidant therapy.
    Full-text · Article · Oct 2013 · Life sciences
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    ABSTRACT: Ethanol exposure during gestation and lactation decreases selenium (Se) intake, disrupting body Se balance and inducing oxidative stress in rat offspring. Selenium-supplemented diet (0.5 ppm) was administered to ethanol-exposed (20% v/v) dams during gestation and lactation. When the dams' pups were 21 days old, the pups' levels of the main hepatic selenoproteins glutathione peroxidase (GPx1 and GPx4) and selenoprotein P (SelP) were measured. The pups were divided into control (C), alcohol (A), control-selenium (CS), and alcohol-selenium (AS) groups. The purpose was to evaluate the effect of the selenium-supplemented diet on the levels of Se deposits present in the livers of their pups. Alcohol decreases hepatic Se deposits, GPx activity, and GPx1 expression; alcohol increases GPx4 and SelP expression. Se was measured by furnace graphite atomic absorption spectrometry, the antioxidant activity of GPx and concentration of hepatic phospholipids (PL) were determined by spectrophotometry, and the selenoprotein expressions were detected by Western blotting. Selenite treatment prevented alcohol's effects of diminishing the Se deposits, GPx activity, and GPx1 expression, while maintaining the high levels of the expression of GPx4 and SelP. These results suggest that depletion of hepatic Se levels in rat pups, caused by ethanol exposure to their dams, affects the synthesis of the 3 main hepatic selenoproteins in different ways, which is related to a decrease in GPx activity and PL concentration, and an increase in serum Se levels. Selenium supplementation to the dams increased the expression of GPx1, GPx4, and SelP in their pups.
    Full-text · Article · Oct 2013 · Alcohol (Fayetteville, N.Y.)
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    ABSTRACT: Selenium (Se), an essential trace metal, is important in both growth and reproduction and is the constituent of different selenoproteins. The glutathione peroxidase (GPx) family is the most studied as it prevents oxidative stress. Liver oxidation is considered as another mechanism involved in low birth weight. Therefore in order to ascertain whether GPx is related to the effects of Se on growth during gestation and lactation, three groups of rat pups were used: control, Se-deficient and Se-supplemented. Morphological parameters and reproductive indices were evaluated. Hepatic Se levels were measured by graphite-furnace atomic absorption while spectrophotometry was used for activity of antioxidant enzymes and oxidative stress markers in liver; and western blotting for expression of hepatic GPx1 and GPx4. The Se-deficient diet increased mortality at birth, decreased viability and survival indices and stunted growth, length and liver development in offspring, thus decreasing hepatic Se levels, GPx, glutathione reductase and catalase activities, while increased superoxide dismutase activity and protein oxidation. The Se-supplemented diet counteracted all of the above results. GPx1 expression was heavily regulated by Se dietary intake; however, although Se dietary deficiency reduced GPx4 expression, this decrease was not as pronounced. Therefore, it can be concluded that Se dietary intake is intimately related to growth, length, and directly regulating GPx activity primarily via GPx1, and secondly to GPx4, thus affecting liver oxidation and development. These results suggesting that if risk of uterine growth retardation is suspected, or neonates with low birth weight presents signs of liver oxidation, may be beneficial know about Se status.
    Full-text · Article · Sep 2013 · Reproduction
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    M L Ojeda · M J Barrero · F Nogales · M L Murillo · O Carreras
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    ABSTRACT: The principal aim of this study was to investigate the oxidative effects of chronic ethanol consumption on the functions of the heart and the kidney and the possible modification of this effect by folic acid supplementation. Moreover, in order to find whether this oxidative profile affects cardiovascular function, parameters such as heart rate and glomerular filtration rate were also assessed. Four experimental groups of rats were used: control, ethanol-exposed, control supplemented with folic acid and ethanol-exposed plus folic acid. Ethanol-exposed rats were subjected to a chronic ethanol treatment (2 months), in which the level of alcohol reaches 30% v/v. Diet and ethanol solution were provided ad libitum, and folic acid supplementation was 8 vs. 2 ppm. Energy intake, creatinine clearance and heart rate were determined. Antioxidant enzyme activity and lipid and protein peroxidation of the kidney and the heart were measured by the spectrophotometric method. Ethanol increases heart size and catalase (CAT) activity and decreases lipid peroxidation in heart without changing heart rate. However, in the kidney, ethanol decreases CAT activity, increases lipid peroxidation and decreases glomerular filtration rate. Folic acid supplementation avoids these situations; it does not, however, improve glomerular function. Chronic ethanol consumption has many effects on the antioxidant enzymatic activity of the heart and the kidney, leading to increased renal lipid peroxidation prevented by folic acid supplementation.
    Preview · Article · May 2012 · Alcohol and Alcoholism
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    ABSTRACT: Chronic alcohol intake is related to hypertension. There are, however, few studies concerning the effect of ethanol upon hydric balance in relation to arterial pressure. Folic acid intake has beneficial effects upon the cardiovascular system decreasing hyperhomocysteinemia, however, more studies imply that it is related with other mechanisms. Therefore, we have studied the effects of chronic alcohol intake (30% v/v) upon hydric-saline balance and hypertension and have found that dietary supplementation with folic acid (8 mg/kg) improves the above parameters. Our study used four experimental groups of rats: control, alcohol, alcohol with folic acid and control with folic acid. In all cases we measured the clearance of Na(+), K(+) and aldosterone; osmolarity in urine, liquid and solid ingestion; homocysteine levels in serum; cardiac frequency and arterial blood pressure. The alcohol intake increases serum aldosterone and homocysteine, which is reflected in an increase in arterial blood pressure. In addition, we have found that alcohol intake reduces both liquid and solid ingestion (causing a malnourishment status), the clearance of creatinine, aldosterone, Na(+) and K(+), and the ratio ClNa(+)/ClCr; it also increases urine osmolarity. Folic acid supplementation increases the clearance of Na(+) and the ratio ClNa(+)/ClCr. Folic acid intake improves the hypertension provoked by alcohol by increasing the aldosterone clearance, drastically reducing the serum levels of this hormone and thus its hypertensor effect.
    Full-text · Article · Feb 2012 · Life sciences
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    ABSTRACT: The nutritional deficiencies provoked by ethanol consumption, during gestation or lactation, can contribute to multiple birth defects in offspring. In order to improve our knowledge about selenium (Se) distribution in pups exposed to ethanol, the present study evaluated the effect of this drug on intestinal development and determined its action on duodenal absorption of selenomethionine (Se-Met). To determinate if supplementation could improve Se absorption and its serum values, we used two antioxidant supplemented regimens on dams, with selenium alone or selenium plus folic acid, and obtained six groups of pups: C (control), A (alcohol), CS (control + Se), AS (alcohol + Se), CFS (control + Se + folic acid) and AFS (alcohol + Se + folic acid). Duodenal Se-Met transport was performed using an in vivo perfusion method. Se levels were measured by graphite furnace atomic absorption spectrometry. The supplemented diets utilized had a positive influence on body growth, duodenal perimeter and Se content in ethanol-exposed pups. Ethanol exposure increased Se-Met duodenal absorption in all pups, supplemented or not, presenting the highest values of maximal velocity (V(max)) compared with their control counterparts. The affinity constant (K(m)) increased according to rank: A>AS>AFS groups. These results suggest that although antioxidant supplementation does not restore Se-Met absorption to normal values, it enhances the affinity of the transporters for the substrate and improves the damage caused by ethanol in the duodenal mucosa.
    No preview · Article · Sep 2011 · Journal of Reproduction and Development
  • M.J. Delgado · F Nogales · M.L. Ojeda · M.L. Murillo · O Carreras
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    ABSTRACT: The present study aims to compare selenium (Se) status in offspring rats born to selenium-deficient and selenium supplemented dams and to analyse Se's influence on intestinal parameters and the intestinal absorption of selenomethionine (Se-Met). Male and female Wistar rats (150-200 g) were randomised in: control (C) (0.1 ppm Se), Se-deficient (SD) (0.01 ppm Se) and Se-supplemented (SS) (0.5 ppm Se) groups; and were mated to obtain their offspring. Se levels in serum, urine and faeces in offspring and in mothers' milk were measured by graphite-furnace atomic absorption spectrometry. Duodenal transport studies in offspring were performed using an in vivo perfusion of different Se-Met concentrations (2, 5, 10, 25, 75 and 150 μM). KEY FINDING: A Se-deficient diet provoked a decrease in the offspring's body weight and intestinal parameters, while the supplemented diet increased these values. Serum Se levels were similar between Se-deficient and control offspring because the urinary excretion of Se was smaller to compensate for Se homeostasis. Intestinal Se-Met absorption obeys the Michaelis-Menten equation with lower apparent constant (K(m)) and maximal velocity (V(max)) in the SD group. However, the C and SS groups presented similar K(m) and different V(max). The V(max) showed greater values in the following order of rank: SS>C>SD groups. Selenium intake deficiencies in offspring lead to the development of compensatory mechanisms in order to normalise serum selenium levels. These mechanisms, however, do not permit normal body development; nor do they regulate intestinal parameters and Se-Met transport.
    No preview · Article · Nov 2010 · Life sciences
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    M.L. Ojeda · K Jotty · F Nogales · M.L. Murillo · O Carreras
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    ABSTRACT: The levels of folic acid and selenium, two nutrients with antioxidant properties, decrease in dams exposed to ethanol during gestation and lactation. This decrease affects their antioxidant balance, and consequently the health of their offspring. In this study we have proved that a supplemented diet with Se (0.5 ppm) or with Se (0.5 ppm) plus folic acid (8 ppm) to ethanol-exposed (20%v/v) dams prevents the ethanol-provoked effects in their offspring's Se deposits. Se levels in milk, serum, urine, faeces and several tissues were measured by graphite-furnace atomic absorption spectrometry. Results show that ethanol decreases Se deposits in pups' heart, liver, kidney and testes. However Se levels in pancreas and in serum were increased by ethanol; it also compromised the weight and the length of the offspring at the end of lactation. Our supplemented diets to ethanol dams increased all of these impaired levels, and restored Se pancreas concentration to a control status. However Se-only therapy mainly displaces Se to serum, kidney and spleen, and co-treatment with Se plus folic acid, mainly displaces Se to liver and brain. This data demonstrate that the qualitative and quantitative Se organ deposits depend on ethanol consumption, Se status, and the presence of other antioxidants.
    Full-text · Article · Sep 2010 · Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association
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    ABSTRACT: The effect of ethanol consumption, either during pregnancy and/or lactation, on the altered metabolism of zinc (Zn) is not well-defined. Therefore, this study was performed to analyse the effect of chronic ethanol exposure on Zn redistribution in dams and offspring during either gestation and/or lactation. We have used three groups of Wistar rat dams: control (CD), ethanol (ED), and pair-fed dams (PD). Some of the newborns were cross-fostered to dams at birth and we formed five experimental groups of offspring: control (CO); those exposed to ethanol during gestation only (GO); those exposed to ethanol during lactation only (LO); those exposed to ethanol during both periods (EO); and pair-fed groups (PO). Zn levels were measured by flame atomic absorption spectrophotometry. Zinc distribution is altered in ED with respect to CD, presenting significantly higher Zn values in the brain and spleen, and lower levels in the liver. However, total organs Zn levels are similar between dams. Ethanol-treated offspring (GO, LO, EO) consumed significantly less Zn than the CO. However, LO and EO showed significantly higher Zn serum levels. Zn distribution was altered in ethanol-treated offspring. GO and LO showed lower Zn levels in liver than CO; GO presents the lowest Zn liver levels. These levels were significantly lower than EO and PO. Ethanol-treated pups present significantly higher spleen and testes values than CO and PO. Total organ Zn levels were significantly lower in GO. Maternal adaptation resulted in organ Zn retention in order to meet the demands of pup's growth in the face of a lower diet intake. However, there was a redistribution of Zn in organ contents. Therefore, the ethanol route administration (via placenta and/or milk) affects Zn redistribution in pups in a different way.
    No preview · Article · Jul 2010 · Journal of Trace Elements in Medicine and Biology
  • M L Ojeda · F Nogales · K Jotty · M J Barrero · M L Murillo · O Carreras
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    ABSTRACT: Nutrients such as folic acid and selenium are decreased in dams exposed to ethanol during gestation and lactation, affecting their metabolism, antioxidant balance, and the future health of their progeny. We will study whether the supplementation of the maternal diet with folate and selenium can prevent ethanol-induced oxidative liver disorders in the offspring. Dams were randomised into four groups: control, alcohol, alcohol+folic acid+Se, and control+folic acid+Se. We determined selenium by graphite-furnace atomic absorption and antioxidant enzyme activities, lipid peroxidation, and protein carbonyl by spectrophotometry in the offspring. Alcohol increased serum Se levels and glutathione peroxidase (GPx) activity. However, in the liver of pups from ethanol-exposed dams a decrease in selenium was provoked and GPx activity increased with the double supplementation. Glutathione reductase (GR) and catalase (CAT) activities increased with ethanol, while double supplementation significantly decreased the GR activity. The supplemented diet reduced the protein peroxidation found in ethanol pups. These results suggest that folic acid+Se could be effective in neutralising the damage of ethanol consumption in pups since it prevents peroxidation protein products.
    No preview · Article · Dec 2009 · Birth Defects Research Part B Developmental and Reproductive Toxicology
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    K Jotty · M.L. Ojeda · F Nogales · J.M. Rubio · M.L. Murillo · O Carreras
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    ABSTRACT: Ethanol consumption affects maternal nutrition and antioxidant status together with the future health of their progeny. Selenium (Se) is a trace element with antioxidant activity; we will study the effect of ethanol in dams on Se bioavailability, antioxidant balance and gestational parameters. We also will study if a Se-supplemented diet (0.5 ppm) administered to ethanol-exposed dams avoids the undesirable effects provoked by ethanol. We have used four experimental groups: control (C); chronic ethanol (A); control+Se (CS) and chronic ethanol+Se (AS). Se levels in serum, urine, faeces, and several tissues were measured by graphite-furnace atomic absorption spectrometry. Serum glutathione peroxidase (GPx) activity was determined by spectrometry. Se bioavailability is altered by ethanol, causing a decrease in Se retention, reducing Se levels in cortex, muscle, mammary gland and salivary gland while elevating Se values in heart, liver and spleen. On the other hand, Se supplementation increases some of these parameters. Serum GPx activity was decreased by ethanol, while a Se-supplemented diet restores these values to those found in controls. We have demonstrated that ethanol decreased Se retention in dams, affecting their tissues' Se deposits, decreasing GPx activity in serum, gestational parameters and the weight of their progeny. Selenite supplementation counteracts these decreasing effects, except in cortex.
    Full-text · Article · Aug 2009 · Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association
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    ABSTRACT: The aim of this paper is to study the relationship between alcohol, selenium and oxidative stress in breastfeeding rat pups exposed to ethanol during gestation and lactation. We have also studied how a Se-supplemented diet among mothers could prevent different oxidative liver disorders in the pups. Pups of 21 days were randomized into four groups: control group (C), alcohol group (A), alcohol selenium group (AS) and control selenium group (CS). Alcohol was supplied to their mothers for 13 weeks (induction, reproduction, gestation and lactation periods). The selenium-supplemented diet contained 0.5 ppm as selenite. We determined serum and liver selenium by graphite-furnace atomic absorption spectrometry. We measured antioxidant enzyme activities: glutathione peroxidase (GPx), glutathione reductase (GR), catalase (CAT) and superoxide dismutase (SOD); and lipid peroxidation (TBARS) and protein carbonyl (PC) by a spectrophotometric method in the liver. In the liver of pups, exposure to ethanol provoked a decrease in selenium and GPx activity and an increase in GR and CAT activity, as well as in carbonyl groups in protein. A pups had higher Se levels and GPx activity in serum than C pups. Administering Se with alcohol balances the activities of scavenging enzymes and reduces peroxidation protein products. These results suggest that selenium could be effective in neutralizing the damage of ethanol consumption during gestation and lactation in pups since it repairs selenium levels in liver as well as the activity of scavenging enzymes and peroxidation protein products. In serum, Se also recovers GPx activity and increases the levels of Se that are available to other organs.
    Preview · Article · Mar 2009 · Alcohol and Alcoholism
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    ABSTRACT: Cited By (since 1996):17, Export Date: 18 October 2014
    No preview · Article · Jan 2009
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    ABSTRACT: In this study we determined whether a folic acid-supplemented diet could change hyperlipaemia provoked by chronic ethanol intake in adult and pup rats. Animals were randomized into eight groups (four adults and four pups): control groups, water and basic diet; alcohol groups, 20% ethanol and basic diet; alcohol folic acid groups, 20% ethanol and diet supplemented with folic acid; control folic acid groups, water and folic acid-supplemented diet. We determined serum and liver total cholesterol (Chol), HDL, triglycerides (TG), phospholipids (PL) and bile acids (BA) levels in all of the groups. Hydroxymethylglutaryl-CoA (HMG-CoA) reductase activity was also measured in the livers. Ethanol-fed rats have higher serum HDL and PL levels in pups and higher serum LDL, TG and PL levels in adults than controls and supplemented animals with or without alcohol ingestion. Ethanol provokes an increase in hepatic Chol and BA, and a decrease in hepatic TG and PL in pups; in adults it also provokes an increase in hepatic Chol and BA and a significant increase in HMG-CoA reductase activity. Alcohol intake plus folic acid supplementation has no effects on these values except BA levels that were significantly higher, in both pups and adult rats, than in the control group. Despite the fact that alcohol intake provokes different lipid alterations in adults and in pups whose mothers drank ethanol, folic acid contributes to the alleviation of these adverse effects reducing HMG-CoA reductase activity in adult rats and, except BA levels, to normalizing lipids values due to the fact that folic acid acts as a choleretic compound. We can therefore assume that folic acid supplementation reduces alcohol-induced hypercholesterolaemia by decreasing synthesis and increasing catabolism.
    Preview · Article · Jun 2008 · Alcohol and Alcoholism
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    ABSTRACT: Ethanol ingestion is known to interfere with folate absorption and metabolism. A fostering/crossfostering analysis of maternal ethanol exposure effects on jejunum and ileum kinetic parameters in vivo of offspring rat folic acid absorption at 21 days postpartum was carried out. The rats were divided into four groups: CP, control pups; GP, pups exposed to ethanol only during gestation; LP, pups exposed to ethanol only during lactation; GLP, pups exposed to ethanol during gestation and lactation. Jejunal and ileal loop transport studies were performed using in vivo perfusion at a flow rate of 3 ml/min for 5 min. Folic acid concentrations of 0.25, 0.5, 1, 1.5 and 2.5 μm were used. Jejunal and ileal absorption values were determined by the difference between the initial and the final amounts of substrate in the perfusate and expressed as picomoles per square centimeter of intestinal surface every 5 min. The results indicated that ethanol consumption by the dams during gestation and/or lactation led to significant changes in V max, with no significant changes in apparent K m. These findings suggest that exposure to ethanol during gestational and suckling periods leads to a general delay in postnatal body weight and that intestinal folate absorption appears to be upregulated in suckling rats, this effect being higher in the LP group.
    No preview · Article · Nov 2007 · Journal of Membrane Biology
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    ABSTRACT: The aim of this study was to study the reverse effect of folic acid administered during gestation and lactation to ethanol-treated dams, on cholecystokinin Cholecystokinin (CCK) stimulus-secretion coupling in pancreatic exocrine secretion in offspring rats. Animals were randomized into three groups: Control group (C) received water and basic diet during pregnancy and lactation period; ethanol-treated rats (E) received ethanol and basic diet; the ethanol+folic acid group (EF) received folic acid supplement concomitantly with ethanol administration. Body and pancreatic weight was lower in offsprings after ethanol treatment. Folic acid supplementation increased these parameters with respect to ethanol rats. After CCK stimulation, a significant decrease in amylase, lipase and chymotrypsin activities in the duodenal juice were detected in ethanol, this trend was partially corrected with folate supplementation. Ethanol exerts its action on exocrine pancreatic secretion by two pathways: 'per se' and diminishing the folic acid content, because a folic acid supplement in rats during pregnancy and lactation periods produces an advantageous effect on amylase, lipase and chymotrypsin secretion in their offspring. Although extrapolation from animal studies may be tenuous, the present findings may explain the use of folic acid in the prevention of ethanol-induced damage by increasing the enzyme levels to adequate physiological concentrations.
    Full-text · Article · May 2007 · Alcohol and Alcoholism
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    ABSTRACT: The effect of ethanol consumption, either during the pregnancy or lactation period, on the altered metabolism of zinc is not well-defined; consequently, this study was performed to analyze the effect of chronic ethanol exposure on milk consumption, serum, milk, duodenal absorption, fecal and urinary excretion of zinc in dams and offspring during either gestation or lactation in the rat. A complementary study was performed regarding pregnancy outcome. We evaluated testosterone values, the offspring born/litter and several indices such as fertility, viable gestations and the survival index. To study the effect of chronic alcoholism during gestation or lactation separately, at birth control newborns were cross-fostered to ethanol dams (ED), and the offspring issued from the ethanol treated mothers were cross-fostered to control dams (CD). Thus, three experimental groups of offspring were formed: (i) control offspring receiving no treatment (CO); (ii) offspring exposed to ethanol only during gestation (GO); and (iii) offspring exposed to ethanol only during lactation (LO). All the results were compared with offspring pair-fed groups (PFO) born of the pair-fed dams (PFD). Duodenal absorption of zinc increased significantly in LO offspring when the substrate concentrations in the perfusion medium were 25, 75, and 150 microM. A higher faecal excretion in GO pups compared with those with LO exposure and control groups (CO and PFO). The urine excretion of zinc was higher for LO offspring with respect to the other three experimental groups (CO, GO, and PFO). Maternal adaptation resulted in zinc retention, adequate to meet the demands of pup's growth in the face of a lower diet intake. The zinc status in pups is regulated by a higher absorption of zinc and intestinal conservation of endogenous fecal zinc after postnatal ethanol consumption. The increase in urinary zinc excretion could be responsible for decreased serum zinc. However, we found an increase in serum zinc probably due to an increase in the zinc absorption values.
    No preview · Article · Oct 2006 · Alcohol and Alcoholism
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    ABSTRACT: S-adenosylmethionine (SAM) is an universal methyl donor for biological systems in transmethylation reactions. Another metabolic pathway involving S-adenosylmethionine is initiated with the release of -CH3 from the molecule and the formation of S-adenosylhomocysteine and then homocysteine and cysteine, a precursor of the main cellular antioxidant glutathione. Chronic ethanol consumption could affect the bioavailability of amino acids such as methionine. Our purpose was to determine the effect of chronic alcohol feeding during gestation or lactation on hepatic S-adenosyl-methionine, S-adenosylhomocysteine, DNA methylation and homocysteine serum concentration at the end of the lactation period (21-day-old offspring). Wistar dam rats were fed with alcohol during periconceptional, gestation and lactation periods (alcohol-fed rats). This study was conducted with three groups of offspring with different periods of alcohol exposure: control offspring (C), no treatment; and gestation (G) and lactation (L) offspring, exposed to alcohol only during gestation or lactation, respectively. To obtain these last two groups of offspring, on parturition day control newborn rats were cross-fostered to alcohol-fed dams (L) and alcohol new-born rats were cross-fostered to control dams (G). In conclusion, these results indicate that exposure of rats to ethanol during the lactation period affects SAM values more severely than ethanol exposure only during gestation.
    No preview · Article · Jul 2005 · Addiction Biology