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Alcohol-Induced Cell Death in the Embryo

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Alcohol-Induced Cell Death in the Embryo Alcohol-Induced Cell Death in the Embryo SUSAN M. SMITH, PH.D. Exposure to alcohol during gestation can have profound consequences, but not all cells within the embryo are affected equally. Recent advances in molecular embryology have allowed an exploration of this variation. Much of this research has focused on the embryo’s vulnerability to the facial malformations characteristic of fetal alcohol syndrome. Studies using mice and chicks show that alcohol exposure at specific stages of early embryo development results in significant death among the cells destined to give rise to facial structures (i.e., cranial neural crest cells). This type of cell death is through activation of the cell’s own “self-destruct” machinery (i.e., apoptosis). Researchers have advanced several theories to explain how alcohol triggers apoptosis in the neural crest cells. These theories include deficiency in a type of vitamin A compound, retinoic acid; reduced levels of antioxidant compounds (i.e., free radical scavengers) that protect against damage from toxic oxygen molecules (i.e., free radicals); and interference with the cell’s normal internal communication pathways. KEY WORDS: congenital facial anomaly; fetal alcohol syndrome; prenatal alcohol exposure; cytolysis; gestation; teratogens; neural cell; temporal context; retinoic acid; free radicals; oxygen; cell signaling; animal model; literature review lcohol is capable of directly are unplanned. By the time these preg- Clarren 1996). An excellent correlation inducing abnormalities during nancies are confirmed, major embryonic exists between these structural malfor- A prenatal development that can events already have occurred. (For a mations (i.e., dysmorphologies) and a lead to lifelong and profound disabili- brief overview of normal embryo de- history of prenatal alcohol exposure. ties (i.e., it is a teratogen1). In fact, velopment, see sidebar, p. 296–297.) Nevertheless, many children born to prenatal exposure to alcohol—the most Early diagnosis and intervention for alcoholic mothers lack these facial prevalent teratogen in Western society— children affected by prenatal alcohol defects, although the children do exhibit is the most common known cause of exposure can reduce their risk for social alcohol-related neurodevelopmental mental retardation and neurobehavioral difficulties later in life (e.g., problems deficits, such as mental retardation, deficits. By conservative estimates, 12 with employment or trouble with the attention deficits, hyperactivity, im- percent of all patients in long-term law resulting from impulsive behavior pulsiveness, and poor judgmental skills. institutionalized care have fetal alcohol and lack of inhibition) (Streissguth et To help define the risks associated syndrome (FAS) (see Stratton et al. al. 1996). Identifying these children with maternal alcohol use during 1996 for an extensive discussion of can be difficult, however. One useful pregnancy, researchers are seeking to FAS). Although the simplest prevention FAS screening tool relies on the follow- understand the mechanisms of alcohol’s strategy is for women to avoid alcohol ing trio of distinctive facial features that teratogenic effects on various tissues. consumption when pregnant or planning characterize prenatal alcohol exposure: to conceive, one-half of all pregnancies small eye openings (i.e., short palpebral SUSAN M. SMITH, PH.D., is an associ- fissures), a thin upper lip, and a flattened ate professor in the Department of 1For a definition of this and other technical or absent groove between the upper lip Nutritional Sciences at the University terms used in this article, see glossary, p. 295. and nose (i.e., philtrum) (Astley and of Wisconsin—Madison. VOL. 21, NO. 4, 1997 287 The use of animal models to reproduce actions and affect only a subset of cells fertilization. For example, alcohol is many of the deficits seen in FAS allows within the embryo. The timing of expo- most likely to cause heart defects investigators to study alcohol’s terato- sure plays a role in the embryo’s outcome during the time when cellular signals genic effects in detail under controlled as well: A given tissue’s susceptibility are directing the heart’s division into treatment conditions. In addition, recent to disruption peaks during distinct its various chambers and great vessels, findings in molecular embryology have timeframes of development (i.e., critical starting 4 weeks after fertilization. greatly advanced scientific knowledge sensitivity windows). Thus, a close In work that was critical in drawing about the signals and agents that govern examination of the target tissue’s devel- attention to alcohol’s early effects on the normal embryo development. Applying opmental history may reveal clues as embryo, Sulik and colleagues (1981) this knowledge can help elucidate how to the toxicant’s mechanism and the used a mouse model developed by prenatal alcohol exposure results in birth basis for the tissue’s sensitivity. Such Webster and colleagues (1980) to defects. It also can clarify our under- examination also may identify addi- convincingly demonstrate that alcohol standing of why certain physical defects tional, previously unsuspected targets. targets early events in organ formation. are useful diagnostics for prenatal alco- For example, because the face, limbs, Using an experimental protocol that hol exposure, and it places these deform- urogenital tract, and central nervous involved exposing mouse embryos to ities within the overall criteria that system all use the same set of genes to alcohol during a specific period of define whether a potentially affected direct their growth and development, gestation (corresponding to the third person may qualify for support services. it is not surprising that certain toxicants week of human pregnancy),2 the research- This article first reviews current or genetic mutations will disrupt all of ers produced facial malformations understanding about the embryo’s these tissues to some degree. consistent with the visible characteris- vulnerability to facial malformations The concept of critical sensitivity tics of FAS in people (i.e., a narrow and the alcohol-induced cell death windows is useful in examining how forehead, short palpebral fissures, a responsible for producing such deform- alcohol produces its teratogenic effects. small nose and midface, and a long ities. The article then explores several Certain embryonic tissues, such as those upper lip with a deficient philtrum), as theories on how alcohol triggers cell of the face, heart, and urogenital tract, shown in figure 1. The peak maternal death in embryos and concludes with appear to be particularly sensitive to blood alcohol concentration (BAC) in a discussion of possible future re- alcohol-induced malformations during the mice used in this research ranged search directions. the processes that establish location, from 0.2 to 0.5 percent; the lower growth, and three-dimensional shape as the tissues develop from their primitive 2 ALCOHOL-INDUCED CELL DEATH origins. In humans, many of these early Protocols with alcohol exposure during other specific periods of gestation produced malfor- developmental events occur during a mations in different body systems (e.g., the Many toxic substances (i.e., toxicants), time when a woman may be unaware heart and limbs), as predicted by the critical including alcohol, are specific in their of her pregnancy, 3 to 6 weeks after windows hypothesis. ABC Narrow forehead Short palpebral fissures Small nose Small midface Long upper lip with deficient (flat) philtrum Figure 1 Similarities of facial defects found in (A) humans and (B) mice exposed prenatally to alcohol. Panel C shows a control mouse fetus not exposed to alcohol. (Photograph courtesy of Kathy K. Sulik.) 288 ALCOHOL HEALTH & RESEARCH WORLD Cell Death in the Embryo BAC levels, in particular, are achiev- able in alcoholics. The fact that alcohol causes similar A. Normal embryo B. Alcohol-exposed embryo facial defects in people and rodents implies that alcohol probably affects Primitive eye embryonic events common to both species. Closer examination of alcohol- Primitive eye exposed mouse embryos revealed Primitive brain significant cell death within specific groups (i.e., populations) of cells, in- Primitive brain cluding the primitive neural and facial Primitive ear tissues. In particular, cell death was observed in a group of cells called the neural crest (see figure 2 for similar Heart Primitive ear cell death in chick embryos) (e.g., Sulik et al. 1988). Rats exposed to alcohol during late gestation or soon after birth experienced a similar death of cells within specific brain regions. The restriction of alcohol- induced cell death to selected brain Primitive regions supports the concept that alcohol spinal column affects specific target tissues. Moreover, the causative relationship between Figure 2 Neural crest cell death in the chick embryo. Panel A shows a normal alcohol and cell death is reinforced by embryo after 48 hours of incubation (corresponding to 22 to 25 days of the fact that several alcohol-affected human gestation), when the dark-stained neural crest cells (see arrows) embryonic tissues later result in body migrate from the primitive brain toward regions of facial development. structures that exhibit malformations Panel B shows a 48-hour embryo that was exposed to alcohol at a critical consistent with underdevelopment. In developmental time (i.e., at 18 to 36 hours of incubation). The diffuse, addition to the characteristic
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