BINGE ALCOHOL ADMINISTRATION ON PREGNANT RATS RESULTS IN DECREASING OF INSULIN LIKE GROWTH FACTOR-1 AND ALDEHYDE DEHYDROGENASE, INCREASING APOPTOSIS INDEX, AND FETAL ALCOHOL SYNDROME IN OFFSPRINGS.

Background: Addiction of alcoholic beverage by early pregnancy women results in fetal alcohol syndrome of her baby. This study aims to investigate fetal alcoholic syndrome due to binge alcoholic drinking by the early pregnant of wistar rat. Methods: This is an experimental study applying posttest only control group design. Wistar Rats were in preconditioning for pregnancy and divided into two groups, i.e. one group was fed with normal feeding and the other group was fed with normal feeding and 40% of ethanol. The off spring then were observed and divided into three groups, i.e. normal fetal, normal fetal from the mother fed with ethanol, and fetal alcoholic syndrome. Insulin like growth factor (IGF-1), aldehyde dehydrogenase (ALDH), apoptosis index, pathology of their brain and heart were observed. The different of all these parameters were then compared by applying one way anova, and considered significant at p < 0.05. Results: In this study we found that there were fetals alcoholic syndrome (FAS) due to the mother of the Wistar Rat fed with ethanol during their pregnancy. There were also a significant different of IGF-1, ALDH, apoptosis index between these three groups (p < 0.05), i.e. normal baby, normal fed with ethanol, and FAS. IGF-1 for these three groups were 56.59±0.52 ng/ml, 55.17±2.41 ng/ml, and 36.64±4.86 ng/ml, respectively. ALDH for the groups were 21.41±2.38 ng/ml, 21.16±4.77 ng/ml, and 17.05±2.68 ng/ml, respectively. Their brain apoptosis indexes were 4.56±0.78, 4.58±1.17, and 7.86±1.31, respectively. Heart apoptosis indexes were found 2.81±1.18, 5.36±1.37, and 7.50±1.43, respectively. Conclusion: Binge alcohol drinking during pregnancy of Wistar Rat results in FAS and identified by decrease of IGF-1, ALDH and increase of brain apoptosis index and heart apoptosis index of the off spring.

[1]  Sharanya Ramachandran. REVERSE SHOULDER PROSTHESIS: REVIEW DARI FITUR IMAGING DAN KOMPLIKASINYA , 2015 .

[2]  Julio C. B. Ferreira,et al.  Targeting aldehyde dehydrogenase 2: new therapeutic opportunities. , 2014, Physiological reviews.

[3]  J. Wands,et al.  Role of central nervous system insulin resistance in fetal alcohol spectrum disorders. , 2010, Journal of population therapeutics and clinical pharmacology = Journal de la therapeutique des populations et de la pharamcologie clinique.

[4]  B. Norrving,et al.  Explorative investigation of biomarkers of brain damage and coagulation system activation in clinical stroke differentiation , 2009, Journal of Neurology.

[5]  D. Crabb,et al.  Acetaldehyde generating enzyme systems: roles of alcohol dehydrogenase, CYP2E1 and catalase, and speculations on the role of other enzymes and processes. , 2007, Novartis Foundation symposium.

[6]  G. Egea,et al.  Novel molecular targets for the prevention of fetal alcohol syndrome. , 2007, Recent patents on CNS drug discovery.

[7]  K. Pahan,et al.  Induction of Glial Fibrillary Acidic Protein Expression in Astrocytes by Nitric Oxide , 2006, The Journal of Neuroscience.

[8]  T. Cudd Animal Model Systems for the Study of Alcohol Teratology , 2005, Experimental biology and medicine.

[9]  J. Wands,et al.  Ethanol inhibits insulin expression and actions in the developing brain , 2005, Cellular and Molecular Life Sciences CMLS.

[10]  D. Crabb,et al.  Overview of the role of alcohol dehydrogenase and aldehyde dehydrogenase and their variants in the genesis of alcohol-related pathology , 2004, Proceedings of the Nutrition Society.

[11]  M. Mattson,et al.  Calcium orchestrates apoptosis , 2003, Nature Cell Biology.

[12]  J. Wands,et al.  Chronic gestational exposure to ethanol impairs insulin-stimulated survival and mitochondrial function in cerebellar neurons , 2002, Cellular and Molecular Life Sciences CMLS.

[13]  J. Renau‐Piqueras,et al.  Ethanol exposure enhances cell death in the developing cerebral cortex: Role of brain‐derived neurotrophic factor and its signaling pathways , 2002, Journal of neuroscience research.

[14]  R. Rubin,et al.  Inhibition of insulin-like growth factor-I signaling by ethanol in neuronal cells. , 2001, Alcoholism, clinical and experimental research.

[15]  C. Ikonomidou,et al.  Neuronal death enhanced by N-methyl-D-aspartate antagonists. , 2000, Proceedings of the National Academy of Sciences of the United States of America.

[16]  L. Caplan Caplan's Stroke: A Clinical Approach , 2000 .

[17]  S. Nagata Apoptotic DNA fragmentation. , 2000, Experimental cell research.

[18]  T. Serafini Finding a Partner in a Crowd Neuronal Diversity and Synaptogenesis , 1999, Cell.

[19]  U. Lendahl,et al.  Abnormal Reaction to Central Nervous System Injury in Mice Lacking Glial Fibrillary Acidic Protein and Vimentin , 1999, The Journal of cell biology.

[20]  J. Olney,et al.  Blockade of NMDA receptors and apoptotic neurodegeneration in the developing brain. , 1999, Science.

[21]  Y. F. Wang,et al.  Polymorphism of ADH and ALDH genes among four ethnic groups in China and effects upon the risk for alcoholism. , 1997, Alcoholism, clinical and experimental research.

[22]  T. Schneider,et al.  Ethanol promotes cell death by inhibition of the insulin-like growth factor I receptor. , 1997, Alcoholism, clinical and experimental research.

[23]  C. Ehlers,et al.  Alcohol Metabolism in Asian-American Men with Genetic Polymorphisms of Aldehyde Dehydrogenase , 1997, Annals of Internal Medicine.

[24]  D. Bredesen REVIEW ■ : Keeping Neurons Alive: The Molecular Control of Apoptosis (Part I , 1996 .

[25]  S. Yin,et al.  Ethanol and acetaldehyde metabolism in chinese with different aldehyde dehydrogenase-2 genotypes. , 1995, Proceedings of the National Science Council, Republic of China. Part B, Life sciences.

[26]  R. Baserga,et al.  Ethanol inhibits the autophosphorylation of the insulin-like growth factor 1 (IGF-1) receptor and IGF-1-mediated proliferation of 3T3 cells. , 1993, The Journal of biological chemistry.

[27]  Julianne L. Conry,et al.  Neuropsychological deficits in fetal alcohol syndrome and fetal alcohol effects. , 1990, Alcoholism, clinical and experimental research.

[28]  G White,et al.  Ethanol inhibits NMDA-activated ion current in hippocampal neurons. , 1989, Science.

[29]  R. Sokol,et al.  FETAL ALCOHOL SYNDROME IS NOW LEADING CAUSE OF MENTAL RETARDATION , 1986, The Lancet.

[30]  R. Baxter The somatomedins: insulin-like growth factors. , 1986, Advances in clinical chemistry.

[31]  S. Varma,et al.  Metabolic aspects of fetal alcohol syndrome. , 1983, Neurobehavioral toxicology and teratology.

[32]  J. Samet,et al.  Epidemiology of fetal alcohol syndrome among American Indians of the Southwest. , 1983, Social biology.