M L Murillo

Universidad de Sevilla, Hispalis, Andalusia, Spain

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Publications (53)112.41 Total impact

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    ABSTRACT: Oxidative imbalance is one of the most important mechanisms to alcohol-induced injury. Acute alcohol exposure induces a great amount of reactive oxygen species during its hepatic metabolism via microsomal ethanol oxidizing system. During adolescence the deliver process is still taking place, therefore ethanol effects differ from that in adults. As binge drinking is the most important ethanol consumption model of ethanol intake used by adolescents, and few is known about its effects on liver, we have used two routes of acute ethanol administration (via oral and via intraperitoneal) in adolescent rats in order to analyze the oxidative damaged caused in peripheral and liver. It has been demonstrated for the first time that binge drinking in adolescent causes periphery oxidation of lipid and DNA, as well as lipid and protein hepatic oxidation, which are related to a lower glutathione peroxidise (GPx) activity, a higher catalase (CAT) activity, and a higher expression of NADPHoxidase, contributing to hepatic damage. In addition, it is also showed that intraperitoneal administration route increases oxidative damage, being probably related to the general stress response generated, that in the case of alcohol-exposed rats by via intraperitoneal, causes higher DNA and protein oxidation related to a higher NADPHoxidase expression and to a higher CAT and superoxide dismutase (SOD) activities. According to these results it were concluded that binge drinking induced hepatic damage during adolescence, at least in part, as consequence of oxidative stress since that the antioxidant mechanism delivered was insufficient to avoid liver oxidation. Alcohol administered via i.p provoked more oxidation in DNA than oral alcohol exposure model.
    Chemical Research in Toxicology 10/2014; · 4.19 Impact Factor
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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.
    Alcohol (Fayetteville, N.Y.) 10/2013; · 2.41 Impact Factor
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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.
    Reproduction 09/2013; · 3.26 Impact Factor
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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.
    Alcohol and Alcoholism 05/2012; 47(4):404-12. · 1.96 Impact Factor
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    ABSTRACT: BACKGROUND: Ethanol (EtOH) exposure during gestation and lactation induces an oxidative stress in offspring. In kidney, the oxidative damage is the primary pathway to alcohol-induced injury. In this study, we have demonstrated that a diet supplemented with selenium (Se) (0.5 ppm) or with Se (0.5 ppm) + folic acid (8 ppm) administered to EtOH-exposed (20% v/v) dams during gestation and lactation prevents the oxidative EtOH-provoked effects in their offspring's kidneys. METHODS: All the studies were performed on 21-day-old pups. Serum, urine, and kidney Se levels were assessed by graphite-furnace atomic absorption spectrometry. Se and creatinine clearance, antioxidant enzyme activities, and lipid and protein peroxidation were determined by a spectrophotometric method in kidney. RESULTS: Dietary supplementation treatments used could not improve the glomerular filtration function altered by EtOH exposure during gestation and lactation; however, they did improve renal Se deposits, renal development, and renal protein content while decreasing lipid and protein oxidation and modifying antioxidant enzymes' activity. CONCLUSIONS: Se or Se + folic acid supplementations improve renal development and protein content and modify antioxidant enzymes' activity, decreasing lipid and protein oxidation after EtOH exposure. In this context, a double-supplemented diet appears to reduce protein peroxidation more efficiently than the Se-only-supplemented one, probably via superoxide dismutase and catalase.
    Alcoholism Clinical and Experimental Research 04/2012; · 3.31 Impact Factor
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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.
    Life sciences 02/2012; 90(9-10):337-42. · 2.56 Impact Factor
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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.
    Journal of Reproduction and Development 09/2011; 57(6):708-14. · 1.76 Impact Factor
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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.
    Life sciences 11/2010; 88(3-4):150-5. · 2.56 Impact Factor
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    ABSTRACT: Levels of antioxidants such as folic acid and selenium decrease in dams exposed to ethanol during gestation and lactation, affecting their antioxidant status, their reproductive function and consequently the health of their progeny. We will study whether a Se (0.5 p.p.m.) plus folic acid (8 p.p.m.) supplemented diet administered to ethanol-exposed dams and male rats prevents the effects provoked by ethanol in Se bioavailability and in their glutathione peroxidase (GPx) activity, thus improving the health of their offspring. Se levels in tissue were measured by graphite-furnace atomic absorption spectrometry and serum GPx activity by spectrophotometry. Results show that ethanol decreases Se retention in dams, affecting their tissues' Se deposits, decreasing serum GPx activity, gestational parameters and the weight of their progeny. Se plus folic acid balance Se bioavailability, something that is especially important during gestation and lactation, and as a direct result, the health of their progeny is improved.
    Alcohol and Alcoholism 10/2010; 45(6):489-94. · 1.96 Impact Factor
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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.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 09/2010; 48(12):3486-91. · 2.99 Impact Factor
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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.
    Birth Defects Research Part B Developmental and Reproductive Toxicology 11/2009; 86(6):490-5. · 1.97 Impact Factor
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    ABSTRACT: Ethanol consumption affects maternal nutrition, the mothers' antioxidant balance and the future health of their progeny. Selenium (Se) is a trace element cofactor of the enzyme glutathione peroxidase (GPx). We will study the effect of ethanol on Se bioavailability in dams and in their progeny. We have used three experimental groups of dams: control, chronic ethanol and pair-fed; and three groups of pups. Se levels were measured by graphite-furnace atomic absorption spectrometry. Serum and hepatic GPx activity was determined by spectrometry. We have concluded that ethanol decreased Se retention in dams, affecting their tissue Se deposits and those of their offspring, while also compromising their progeny's weight and oxidation balance. These effects of ethanol are caused by a reduction in Se intake and a direct alcohol-generated oxidation action.
    International Journal of Environmental Research and Public Health 09/2009; 6(8):2139-49. · 1.99 Impact Factor
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    ABSTRACT: Cholesterol metabolism is altered by chronic ethanol consumption. In previous articles, we demonstrated the anti-oxidant capacity of folic acid, which may be useful in the prevention of damage provoked by ethanol. We want to determine the effects of ethanol on cholesterol and bile metabolism and whether a folic acid-supplemented diet could change alterations provoked by a chronic ethanol intake in rats. We used four experimental groups: (1) control, (2) alcohol, (3) alcohol supplemented with folic acid, and (4) control supplemented with folic acid. In all the experimental groups, we measured hepatic 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, and cholesterol and bile acids in serum, liver, bile, and feces. We have found that the alcohol-fed groups showed high hepatic HMG-CoA reductase activity, total hepatic and serum cholesterol concentration, bile cholesterol secretion concentration, and cholesterol enterohepatic circulation. Total serum and hepatic cholesterol levels decreased when alcohol-fed rats were supplemented with folic acid. The hepatic bile acid concentration increased in both chronic ethanol groups. Folic acid supplementation significantly increased bile cholesterol secretion, the bile acids in bile, and fecal bile acid excretion in ethanol-exposed rats. The independent bile acid fraction showed no significant differences between both ethanol groups with respect to Na+, K+, and Cl- concentrations. Folic acid increases bile flow, bile acid synthesis from cholesterol, and bile acid excretion via feces, thus provoking a decrease in serum and hepatic cholesterol. However none of these actions were observed in supplemented control rats. This, therefore, could be yet another beneficial effect of folic acid on alcoholic patients.
    Journal of studies on alcohol and drugs 08/2009; 70(4):615-22. · 1.68 Impact Factor
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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.
    Food and chemical toxicology: an international journal published for the British Industrial Biological Research Association 08/2009; 47(10):2484-9. · 2.99 Impact Factor
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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 microM: 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.
    Journal of Membrane Biology 11/2007; 219(1-3):63-9. · 2.17 Impact Factor
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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.
    Alcohol and Alcoholism 05/2007; 42(4):277-84. · 2.09 Impact Factor
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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.
    Alcohol and Alcoholism 10/2006; 42(1):3-10. · 2.09 Impact Factor
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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.
    Addiction Biology 07/2005; 10(2):139-44. · 5.91 Impact Factor
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    ABSTRACT: This study was designed to examine the effects of ethanol withdrawal on offspring rats that consumed ethanol during gestation and lactation, in order to examine whether there was an improvement in pancreatic trypsinogen and lipase activities at 2 months postpartum with respect to offspring that fed on ethanol until death. A second purpose for our study was to determine if a folic acid supplement during gestation and lactation was sufficient or insufficient to reverse the negative effects of ethanol consumption. Both genders were used with the aim of investigating any differential pancreatic behaviour. The animals were randomized into five groups: the control group (CG) received water and a basic rat diet during pregnancy, lactation and growth; the ethanol group (EG) was fed an ethanol diet during pregnancy, the suckling period and growth until death; the ethanol-water group's (E+WG) ethanol was eliminated after lactation; The ethanol-folic acid group (E+FG) received a folic acid supplemented diet during pregnancy and the suckling period and in the ethanol+folic acid group (E+FG+FG) this supplementation continued during growth. Our results showed that ethanol administration or ethanol withdrawal did not significantly alter lipase activity in the pancreas. Ethanol administration decreased trypsinogen levels in the pancreas of males and females. However, in males, as opposed to females, the withdrawal of ethanol did not recover the values of pancreatic trypsinogen content, nor did a folic acid supplementation significantly alter the parameters we studied. Our treatment produced no effect on lipase levels. There was a gender-related difference in pancreatic trypsinogen content, the implication being that in future all results on exocrine pancreas function in male and female animals should be analysed separately.
    Addiction Biology 09/2004; 9(3-4):239-46. · 5.91 Impact Factor
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    ABSTRACT: The present study was designed to determine whether folic acid supplement is sufficient to reverse the negative effects of ethanol consumption on amylase activity during gestation, lactation, and growth. Moreover, this study investigated the sex-related differences in amylase content in the pancreatic tissue, serum, and urine. The animals were randomized into three groups: Control group (CG) received water and a basic rat diet during pregnancy, lactation, and growth; Ethanol-rats (EG) were fed an ethanol diet during pregnancy, the suckling period, and growth until death; and Ethanol + folic acid group (E + FG) were handled the same way as those of EG, except they received a folic acid supplement from reproduction until the end of experimental period. Our results showed that ethanol consumption decreased the pancreatic amylase level in offspring rats at 2 months postpartum. Folic acid supplementation did not alter pancreatic amylase activities. In offspring males, ethanol administration decreased serum amylase activity at 2 months postpartum. Folic acid supplementation in males resulted in higher serum amylase levels than those corresponding to the ethanol-fed group. In females, no significant differences between groups in serum amylase levels were found. Ethanol consumption decreased urinary amylase excretion (at 30 days and 2 months postpartum), but the folic acid-supplemented group showed a more pronounced decrease in urine amylase activity than in the ethanol-fed group. At 30 days postpartum, no sex difference in urinary amylase was identified. However, in general, males showed higher values for urine amylase than females at 2 months postpartum. A folic acid-supplemented diet exerts an advantageous effect on amylase in serum in offspring males at 2 months postpartum of mothers fed ethanol during gestation and lactation periods, because amylase renal absorption is increased. In offspring females, amylase renal absorption is also increased, but we did not observed an advantageous effect on amylase in serum. It may be that sexual differentiation in females at 2 months postpartum exerts a definitive effect on amylase in serum. We found a sex-related difference in amylase activities; therefore, we suggest that in future all results of the exocrine pancreas function, in male and female animals, be analyzed separately.
    International Journal for Vitamin and Nutrition Research 02/2004; 74(1):64-75. · 1.00 Impact Factor

Publication Stats

247 Citations
112.41 Total Impact Points

Institutions

  • 1986–2013
    • Universidad de Sevilla
      • • Departamento de Zoología
      • • Departamento de Fisiología
      • • Facultad De Farmacia
      • • Departamento de Bioquímica Médica Y Biología Molecular
      Hispalis, Andalusia, Spain