Protective influence of zinc against the deleterious effects of ethanol in postimplantation rat embryos in vivo

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

“…However, it must be noted that the neuronal loss, specifically of the cerebellar Purkinje cells, is only one of the manifestations associated with alcohol-mediated teratogenesis. It has been reported that zinc supplementation may protect against the damaging effects of alcohol on cerebral and cardiac development (Seyoum and Persaud, 1995;Tanaka, 1998), even though the current findings showed that zinc supplementation did not attenuate alcoholinduced cerebellar Purkinje cell loss. Perhaps the most important point to be gleaned from the present study is that alcohol exposure that produces peak blood alcohol concentration that reach 300 mg/dl during part of the third trimester equivalent produces cerebellar Purkinje cell loss that appears to involve a mechanism that is independent of serum zinc levels.…”

Dietary Zinc Supplementation Throughout Pregnancy Protects Against Fetal Dysmorphology and Improves Postnatal Survival After Prenatal Ethanol Exposure in Mice

“…One possible example is cardiac malformations, as a study identical to ours demonstrated that ethanol exposure on GD 8 resulted in 60% of fetuses developing ventricular septal defects (Webster et al., 1984). In this regard, it has been shown that embryos from rats treated with ethanol and Zn had more advanced cardiac development compared to those treated with ethanol alone (Seyoum and Persaud, 1995). Thus, further studies are warranted to examine the effect of ethanol and dietary Zn supplementation throughout pregnancy on other internal body systems.…”

“…Seyoum and Persaud (1995) were the first to show that Zn treatment could protect against ethanol teratogenicity. They found that an intraperitoneal injection of Zn given at the time of ethanol exposure in rats resulted in a higher number of somites and embryonic protein content, and that fetal cardiac development was more advanced than ethanol treatment alone.…”

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

“…Critical to the current article, in rodent models, acute alcohol exposure is associated with APR‐induced reductions in fetal Zn uptake [62, 89–91, 95, 96]. That the above reductions in fetal Zn uptake are functionally significant is suggested by the observation that the teratogenicity of alcohol is lessened when animals are given Zn before the alcohol exposure [95–98]. Moreover, the teratogenicity of acute alcohol exposure is reduced in metallothionein knockout mice compared with metallothionein wild‐type mice [90].…”