Selenium or Selenium Plus Folic Acid–Supplemented Diets Ameliorate Renal Oxidation in Ethanol‐Exposed Pups

Ojeda, María Luisa; Nogales, Fátima; Murillo, María Luisa Ojeda; Carreras, Olimpia

doi:10.1111/j.1530-0277.2012.01788.x

Cited by 16 publications

(16 citation statements)

References 50 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In accordance with these data, GPx activity and Se levels in liver decreased analogously in SD pups and increased at a similar rate in SS pups. This direct relationship between Se and GPx activity in liver was also found by other authors in different tissues (Agay et al 2005, Ojeda et al 2012.…”

Section: Antioxidative Defense and Oxidative Stress Markers In Liversupporting

confidence: 69%

Role of selenium and glutathione peroxidase on development, growth, and oxidative balance in rat offspring

Nogales¹,

Ojeda²,

Fenutría³

et al. 2013

Reproduction

Self Cite

View full text Add to dashboard Cite

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 (SD), and Se supplemented (SS). 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 SD 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 increasing superoxide dismutase activity and protein oxidation. The SS diet counteracted all 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 suggest that if risk of uterine growth retardation is suspected, or if a neonate with low birth weight presents with signs of liver oxidation, it may be beneficial to know about Se status.

show abstract

Section: Antioxidative Defense and Oxidative Stress Markers In Liversupporting

confidence: 69%

Role of selenium and glutathione peroxidase on development, growth, and oxidative balance in rat offspring

Nogales¹,

Ojeda²,

Fenutría³

et al. 2013

Reproduction

Self Cite

View full text Add to dashboard Cite

show abstract

“…Therefore, although serum Se levels were higher, the SelP/Se serum ratio was lower, showing that in Se-supplemented pups (CS and AS), the excess SelP synthesized in the liver remains in this tissue as the main selenoprotein reservoir. In addition, there is another Se transporter in serum, probably GPx3, that increases Se serum levels (Ojeda, Nogales, Murillo, & Carreras, 2012). With this kind of Se supplementation (an inorganic form: selenite), the GPx3 activity was improved.…”

Section: Discussionmentioning

confidence: 98%

Selenium dietary supplementation as a mechanism to restore hepatic selenoprotein regulation in rat pups exposed to alcohol

Jotty

Ojeda

Nogales

et al. 2013

Alcohol

Self Cite

View full text Add to dashboard Cite

“…In kidney, however, and despite the Se depletion found, the GPx activity value was similar to control pups. The explanation for this is that the kidney is the main tissue for synthesizing extracellular GPx (GPx3) (Whitin et al 2002), so the activity measured was due to the activity of GPx1 and GPx3 (Ojeda et al 2012). Perhaps GPx1 expression is downregulated since it depends on Se levels, and GPx3 is upregulated in kidney because this tissue is the main producer of GPx3.…”

Section: Pre-and Postnatal Alcohol Exposure: Effects On Selenium Balamentioning

confidence: 99%

“…Therefore, in order to avoid future oxidative damage to them and their progeny, a controlled supplementary Se antioxidant therapy would appear to be recommendable for mothers who consume ethanol during gestation and lactation. In this context different studies have analyzed with different objectives the effects of Se supplementation (0.5ppm of sodium selenite) upon both ethanol-exposed dams during gestation and lactation and their offspring in order to improve their oxidative balance (Ojeda et al 2009b;Ojeda et al 2009c;Ojeda et al 2012); to analyze their intestinal Se-Met absorption (Nogales et al 2011); to evaluate Se absorption, retention and body distribution (Jotty et al 2009;Ojeda et al 2010a, Ojeda et al 210b), and to study selenoprotein liver expression (Jotty et al 2013). These studies confirm that Se supplementations improve the transporter's affinity to substrates needed for Se-methionine absorption and minimize the ethanol-induced damage in the duodenal mucosa, improving Se bioavailability in pups and even improving their nutritional status (Nogales et al 2011).…”

Section: R a F Tmentioning

confidence: 99%

The role of folic acid and selenium against oxidative damage from ethanol in early life programming: a review

Ojeda

Nogales

Murillo

et al. 2018

Biochem. Cell Biol.

Self Cite

View full text Add to dashboard Cite

There are disorders in children, covered by the umbrella term "fetal alcohol spectrum disorder" (FASD), that occur as result of alcohol consumption during pregnancy and lactation. They appear, at least in part, to be related to the oxidative stress generated by ethanol. Ethanol metabolism generates reactive oxygen species and depletes the antioxidant molecule glutathione (GSH), leading to oxidative stress and lipid and protein damage, which are related to growth retardation and neurotoxicity, thereby increasing the incidence of FASD. Furthermore, prenatal and postnatal exposure to ethanol in dams, as well as increasing oxidation in offspring, causes malnutrition of several micronutrients such as the antioxidant folic acid and selenium (Se), affecting their metabolism and bodily distribution. Although abstinence from alcohol is the only way to prevent FASD, it is possible to reduce its harmful effects with a maternal dietary antioxidant therapy. In this review, folic acid and Se have been chosen to be analyzed as antioxidant intervention systems related to FASD because, like ethanol, they act on the methionine metabolic cycle, being related to the endogenous antioxidants GSH and glutathione peroxidase. Moreover, several birth defects are related to poor folate and Se status.

show abstract

Selenium or Selenium Plus Folic Acid–Supplemented Diets Ameliorate Renal Oxidation in Ethanol‐Exposed Pups

Cited by 16 publications

References 50 publications

Role of selenium and glutathione peroxidase on development, growth, and oxidative balance in rat offspring

Role of selenium and glutathione peroxidase on development, growth, and oxidative balance in rat offspring

Selenium dietary supplementation as a mechanism to restore hepatic selenoprotein regulation in rat pups exposed to alcohol

The role of folic acid and selenium against oxidative damage from ethanol in early life programming: a review

Contact Info

Product

Resources

About