Oxidative Effects in Early Stages of Embryo Development Due to Alcohol Consumption

被引:4
作者
Gonzalez-Flores, David [1 ]
Marquez, Antonia [1 ]
Casimiro, Ilda [2 ]
机构
[1] Univ Extremadura, Fac Med & Hlth Sci, Dept Anat Cell Biol & Zool, Badajoz 06006, Spain
[2] Univ Extremadura, Fac Sci, Dept Anat Cell Biol & Zool, Badajoz 06006, Spain
关键词
ethanol; FASD; developmental biology; fetus; oxidative stress; PRENATAL ETHANOL EXPOSURE; SPECTRUM DISORDER; DNA METHYLATION; GENE-EXPRESSION; LIVER-DISEASE; MEMORY CONSOLIDATION; ANTIOXIDANT ENZYMES; INSULIN-RESISTANCE; IGF2; EXPRESSION; TNF-ALPHA;
D O I
10.3390/ijms25074100
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Alcohol, a widely consumed drug, exerts significant toxic effects on the human organism. This review focuses on its impact during fetal development, when it leads to a spectrum of disorders collectively termed Fetal Alcohol Spectrum Disorders (FASD). Children afflicted by FASD exhibit distinct clinical manifestations, including facial dysmorphism, delayed growth, and neurological and behavioral disorders. These behavioral issues encompass diminished intellectual capacity, memory impairment, and heightened impulsiveness. While the precise mechanisms underlying alcohol-induced fetal damage remain incompletely understood, research indicates a pivotal role for reactive oxygen species (ROS) that are released during alcohol metabolism, inciting inflammation at the cerebral level. Ethanol metabolism amplifies the generation of oxidant molecules, inducing through alterations in enzymatic and non-enzymatic systems responsible for cellular homeostasis. Alcohol consumption disrupts endogenous enzyme activity and fosters lipid peroxidation in consumers, potentially affecting the developing fetus. Addressing this concern, administration of metformin during the prenatal period, corresponding to the third trimester of human pregnancy, emerges as a potential therapeutic intervention for mitigating FASD. This proposed approach holds promise for ameliorating the adverse effects of alcohol exposure on fetal development and warrants further investigation.
引用
收藏
页数:21
相关论文
共 143 条
[1]   The Impact of Prenatal Ethanol Exposure on Neuroanatomical and Behavioral Development in Mice [J].
Abbott, Charles W. ;
Kozanian, Olga O. ;
Kanaan, Joseph ;
Wendel, Kara M. ;
Huffman, Kelly J. .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 2016, 40 (01) :122-133
[2]   A guideline for the prevention and management of Fetal Alcohol Spectrum Disorder in South Africa [J].
Adebiyi, Babatope O. ;
Mukumbang, Ferdinand C. ;
Beytell, Anna-Marie .
BMC HEALTH SERVICES RESEARCH, 2019, 19 (01)
[3]   Effect of moderate alcohol intake on lipid peroxidation in plasma, erythrocyte and leukocyte and on some antioxidant enzymes [J].
Akkus, I ;
Gültekin, F ;
Aköz, M ;
Çaglayan, O ;
Bahçaci, S ;
Can, ÜG ;
Ay, M ;
Gürel, A .
CLINICA CHIMICA ACTA, 1997, 266 (02) :141-147
[4]   Metformin Reduces Endogenous Reactive Oxygen Species and Associated DNA Damage [J].
Algire, Carolyn ;
Moiseeva, Olga ;
Deschenes-Simard, Xavier ;
Amrein, Lilian ;
Petruccelli, Luca ;
Birman, Elena ;
Viollet, Benoit ;
Ferbeyre, Gerardo ;
Pollak, Michael N. .
CANCER PREVENTION RESEARCH, 2012, 5 (04) :536-543
[5]   The Impact of Alcoholic Beverages on Human Health [J].
Anderson, Peter .
NUTRIENTS, 2021, 13 (12)
[6]  
Aros S, 2008, REV CHIL PEDIATR-CHI, V79, pS46
[7]   Lipid Peroxidation: Production, Metabolism, and Signaling Mechanisms of Malondialdehyde and 4-Hydroxy-2-Nonenal [J].
Ayala, Antonio ;
Munoz, Mario F. ;
Argueelles, Sandro .
OXIDATIVE MEDICINE AND CELLULAR LONGEVITY, 2014, 2014
[8]  
Bejarano Ignacio, 2009, Int J Biomed Sci, V5, P246
[9]   Gestational Choline Supplementation Normalized Fetal Alcohol-Induced Alterations in Histone Modifications, DNA Methylation, and Proopiomelanocortin (POMC) Gene Expression in -Endorphin-Producing POMC Neurons of the Hypothalamus [J].
Bekdash, Rola A. ;
Zhang, Changqing ;
Sarkar, Dipak K. .
ALCOHOLISM-CLINICAL AND EXPERIMENTAL RESEARCH, 2013, 37 (07) :1133-1142
[10]   Animal models of gene-alcohol interactions [J].
Ben Lovely, Charles .
BIRTH DEFECTS RESEARCH, 2020, 112 (04) :367-379