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

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

doi:10.1016/j.alcohol.2013.07.004

Cited by 15 publications

(17 citation statements)

References 40 publications

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“…The study investigated the effect of alcoholic beverages on the parameters of oxidative stress in the liver of adolescent male rats. A number of studies have been conducted in animal models to analyze the influence of alcohol overconsumption on the hepatic damage during adolescence [27], or the damage occurring in progeny due to alcohol consumption by the mother [28]. However, most of the studies focusing on adolescent organisms considered only binge drinking, and not prolonged drinking, as it was justified that binge drinking is the most common way of ethanol intake among adolescents [27].…”

Section: Discussionmentioning

confidence: 99%

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

et al. 2020

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Typical alcohol consumption begins in the adolescence period, increasing the risk of alcoholic liver disease (ALD) in adolescents and young adults, and while the pathophysiology of ALD is still not completely understood, it is believed that oxidative stress may be the major contributor that initiates and promotes the progression of liver damage. The aim of the present study was to assess the influence of alcohol consumption on the markers of oxidative stress and liver inflammation in the animal model of prolonged alcohol consumption in adolescents using various alcoholic beverages. In a homogenic group of 24 male Wistar rats (4 groups—6 animals per group), since 30th day of life, in order to mimic the alcohol consumption since adolescence, animals received (1) no alcoholic beverage (control group), (2) ethanol solution, (3) red wine, or (4) beer (experimental groups) for 6 weeks. Afterwards, the activities of alcohol dehydrogenase (ADH), alanine aminotransferase (ALT), and aspartate aminotransferase (AST), as well as levels of cytochrome P450-2E1 (CYP2E1), thiobarbituric acid-reactive substances (TBARS), protein carbonyl groups, tumor necrosis factor-α (TNF-α), and interleukine-10 (IL-10) were measured in liver homogenates. The difference between studied groups was observed for CYP2E1 and protein carbonyl groups levels (increased levels for animals receiving beer compared with control group), as well as for ALT activity (decreased activity for animals receiving beer compared with other experimental groups) (p < 0.05). The results suggested that some components of beer, other than ethanol, are responsible for its influence on the markers of oxidative stress and liver inflammation observed in the animal model of prolonged alcohol consumption in adolescents. Taking this into account, beer consumption in adolescents, which is a serious public health issue, should be assessed in further studies to broaden the knowledge of the progression of liver damage caused by alcohol consumption in this group.

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Section: Discussionmentioning

confidence: 99%

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

et al. 2020

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“…However, the antioxidant reagent N-acetylcysteine (NAC) significantly inhibited the ethanol-associated apoptosis and recovery of retinal cells from ethanol induced zebrafish embryos [25]. The selenium supplemented diet in ethanol treated dams could be effective in neutralising the ethanol damage in pups and selenium restored hepatic liver cell[38].…”

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confidence: 99%

Sodium selenite/selenium nanoparticles (SeNPs) protect cardiomyoblasts and zebrafish embryos against ethanol induced oxidative stress

Kalishwaralal

Jeyabharathi

Sundar

et al. 2015

Journal of Trace Elements in Medicine and Biology

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“…Therefore, ethanolexposed dams tend to retain more Se in spleen, heart and liver at the expense of other tissue (mainly skeletal muscle), probably to improve oxidative balance via GPx expression in those organs, the liver being the main tissue damaged by pro-oxidative alcohol action (Jotty et al 2009). Despite this corporal redistribution of maternal Se deposits, milk Se levels were lower in ethanol-exposed dams (Jotty et al 2013). Moreover, weaning pups intake less milk and ethanol alters their intestinal absorption decreasing the pups' intestinal perimeter, as well as its length and weight (Nogales et al 2011, Bhalla et al 2004, even affecting the Se-methionine D r a f t transport system.…”

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

confidence: 96%

“…Since Gpx proteins have different biological implications, Jotty et al (2013) studied the expression of the three main hepatic selenoproteins Gpx1, Gpx4 and SelP (Hoffmann et al 2007) in the liver of ethanol-exposed pups during gestation and lactation in order to increase knowledge about the biological implication of Se. The liver is the main ethanol-metabolizing tissue which receives the oxidative products generated by this drug (Lieber 2003).…”

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.

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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.

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

Cited by 15 publications

References 40 publications

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

Oxidative Stress Parameters in the Liver of Growing Male Rats Receiving Various Alcoholic Beverages

Sodium selenite/selenium nanoparticles (SeNPs) protect cardiomyoblasts and zebrafish embryos against ethanol induced oxidative stress

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

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