Zinc Supplementation Does Not Attenuate Alcohol-Induced Cerebellar Purkinje Cell Loss During the Brain Growth Spurt Period

Chen, Wei‐Jung A.; Berryhill, Eve C.; West, John C

doi:10.1097/00000374-200104000-00018

Cited by 4 publications

(3 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In support of this concept, Zn given by injection [107] as well as the feeding of diets high in Zn [108] have been reported to reduce neurobehavioral abnormalities in mouse and rat offspring of ethanol‐exposed dams. Although these data are compelling, others, using a rat model, did not observe a protective effect of Zn supplementation on alcohol‐induced developmental brain abnormalities [109]. In addition, it is important to note that there can be adverse interactions among nutrients.…”

Section: Alcohol–zn Interactionsmentioning

confidence: 99%

The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

Keen

Uriu‐Adams

Skalny³

et al. 2010

BioFactors

View full text Add to dashboard Cite

There is increasing evidence that human pregnancy outcome can be significantly compromised by suboptimal maternal nutritional status. Poor diet results in a maternal-fetal environment in which the teratogenicity of other insults such as alcohol might be amplified. As an example, there is evidence that zinc (Zn) can interact with maternal alcohol exposure to influence the risk for fetal alcohol spectrum disorders (FASD). Studies with experimental animals have shown that the teratogenicity of alcohol is increased under conditions of Zn deficiency, while its teratogenicity is lessened when animals are given Zn supplemented diets or Zn injections prior to the alcohol exposure. Alcohol can precipitate an acute phase response resulting in a subsequent increase in maternal liver metallothionein, which can sequester Zn and lead to decreased Zn transfer to the fetus. Importantly, the teratogenicity of acute alcohol exposure is reduced in metallothionein knockout mice, which can have improved Zn transfer to the conceptus relative to wild-type mice. Consistent with the above, Zn status has been reported to be low in alcoholic women at delivery. Preliminary data from two basic science and clinical nutritional studies that are ongoing as part of the international Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD) support the potential role of Zn, among other nutritional factors, relative to risk for FASD. Importantly, the nutrient levels being examined in these studies are relevant to general clinical populations and represent suboptimal levels rather than severe deficiencies. These data suggest that moderate deficiencies in single nutrients can act as permissive factors for FASD, and that adequate nutritional status or intervention through supplementation may provide protection for some of the effects of prenatal alcohol exposure.

show abstract

Section: Alcohol–zn Interactionsmentioning

confidence: 99%

The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

Keen

Uriu‐Adams

Skalny³

et al. 2010

BioFactors

View full text Add to dashboard Cite

show abstract

“… 80 , 81 Alcohol (4.5 g/kg/day; PD4–9) exposure in rat pups during the brain development period resulted in cerebellar Purkinje cell loss, and zinc supplementation (0.54 mg/mL diet) did not rescue alcohol-induced developmental cerebellar Purkinje cell loss. 82 …”

Section: Maternal Micronutrient and Fetal Development During Alcohol ...mentioning

confidence: 99%

Effects of nutrition and gestational alcohol consumption on fetal growth and development

Naik

Lee

et al. 2022

Nutrition Reviews

View full text Add to dashboard Cite

Fetal alcohol exposure can lead to a range of developmental disorders, including impaired fetal growth and development of multiple organ systems. These disorders are grouped under the term fetal alcohol spectrum disorders (FASDs). Adequate nutrition and a conducive intrauterine environment are essential for healthy fetal development. Nutrient deficiencies resulting from inadequate maternal nutrient ingestion may be compounded by alcohol-induced altered nutrient metabolism, placental clearance, and malabsorption. Alcohol-induced alteration of the intrauterine environment is the main source of developmental deficits and nutritional insufficiencies can worsen the effects on fetal development. In this review, we discuss studies examining the collective and interactive effects of nutrition (specifically iron, selenium, vitamin A, thiamine, zinc, folate, vitamin B12, choline, and amino acids) relative to gestational alcohol consumption and its effects on fetal growth and development. We also summarize scientific reports that tested potential benefits of micronutrient supplementation in animal models of fetal alcohol spectrum disorders and in humans. In summary, the deleterious effects of alcohol exposure in relation to nutrient homeostasis further validate that avoidance of alcohol consumption during pregnancy is the most effective way to mitigate the teratogenic effects of alcohol.

show abstract

“…Exposure to EtOH has been known to cause morphological changes, degeneration and neuronal loss in specific parts of the CNS (Paula-Barbosa et al 1991;Lukoyanov et al 2000). Studies with rats have shown that alcohol causes neuronal loss in cerebellum (Chen et al 2001), basal forebrain (Arendt et al 1988), hippocampal formation (PaulaBarbosa et al 1993) and neocortex (Cadete-Leite et al 1990). Excessive EtOH consumption may lead to cognitive dysfunction (Charness 1993;Lukoyanov et al 2000).…”

Section: Assessment Of the Apoptosis On The Basis Of Tunel Assaymentioning

confidence: 99%

Granule Cell Apoptosis Induced by Overdose Copper and Ethanol Is Counterbalanced by Co-Induced Cellular Proliferation in Rat Dentate Gyrus

Akdoğan

Adiguzel

Turgut

et al. 2005

Tohoku J. Exp. Med.

View full text Add to dashboard Cite

Zinc Supplementation Does Not Attenuate Alcohol-Induced Cerebellar Purkinje Cell Loss During the Brain Growth Spurt Period

Cited by 4 publications

References 31 publications

The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

The plausibility of maternal nutritional status being a contributing factor to the risk for fetal alcohol spectrum disorders: The potential influence of zinc status as an example

Effects of nutrition and gestational alcohol consumption on fetal growth and development

Granule Cell Apoptosis Induced by Overdose Copper and Ethanol Is Counterbalanced by Co-Induced Cellular Proliferation in Rat Dentate Gyrus

Contact Info

Product

Resources

About