##s Cysteine ( Cys ) And GSH?

The science behind FAS is quite simple; as it is known that alcohol has a damaging effect on the body, it has similar consequences on the fetus. Since the fetus is constantly developing, the alcohol causes more serious defects to the unborn child. Alcohol exposure to a fetus is known as a teratogen. “Teratogens are substances or conditions that disrupt typical development in offspring as a result of gestational exposure and cause birth defects.” (Wilson & Fraser, 1977). Although the exposure to alcohol causes problems in the fetus, studies have shown that it may not accurately be the alcohol in the mother’s system that causes these defects, rather the byproducts that form when the body metabolizes the alcohol. This can lead to a decrease in brain cells, abnormal location of neurons, and gross malformation to the brain. Since alcohol causes this central nervous system damage, it is classified as a neurobehavioral teratogen, which is a group of teratogens that cause brain damage and modify behaviors. (Riley & Vorhees, 1986). The CNS damage is the primary defect due to alcohol and it is quite common to have these damages without any physical abnormalities. The more alcohol that is consumed the more birth defects that will arise in the

The term “Fetal Alcohol Spectrum disorders” (FASDS) is used to describe the numerous problems associated with exposure to alcohol before birth. Each year in the United States, up to 40,000 babies are born with “Fetal Alcohol Spectrum disorders” (FASDs) (Substance Abuse and Mental Health Services Administration). Additionally, Fetal Alcohol Spectrum disorders (FASDs) comes with effects that range from mild to severe. These effects include mental retardation; learning, emotional and behavioral problems; and defects involving the heart, face and other organs. According to the U.S. Surgeon General, the patterns of drinking that place a baby at greatest risk for FASDS are binge drinking and drinking seven or more drinks per week (Surgeon General). However, FASDS can occur in babies of women who drink less. There is no way of measuring how much alcohol one can consume before defects occur, and no proof that small amounts of alcohol are safe. As little as one drink a day can cause a baby some degree of harm and interfere with their normal development.

333). Clearly the incidence of this syndrome could be greatly reduced, and possibly prevented, through education on the topic. This paper will present the metabolic basis of Fetal Alcohol Syndrome, the pathogenic basis for brain and facial anomalies associated with FAS, and the effects of maternal alcohol consumption on the immune system. Characteristics of diagnosing FAS will follow the discussion of those factors causing the symptoms of this disease.

Within the foetus, embryonic nerve cells grow exponentially, then migrate to their destinations and develop into a vast collection of distinctive neuronal cell categories unique to their specific function. In prearranged patterns, the cells later form networks with other brain cells. The metabolic process of alcohol instigates makes the cells vulnerable to cell damage by free radicals (harmful substances). Research has suggested that “free radical damage can kill sensitive populations of brain cells at critical times of development in the first trimester of pregnancy (Cartwright, M.M).” Additional experiments have suggested that the third trimester is a particularly susceptible stage for damage to brain cells linked to FASD. The metabolic breakdown of alcohol interferes with brain development through the alteration of the function or production of natural regulatory substances that assist in the promotion of the differentiation and orderly growth of

Epilepsy is one of the most common neurodegenerative disorders that affect around 1% of the global population worldwide. Although the optimal use of the 24 approved anti-epileptic drugs in The United States has successfully treat some of the symptoms-related epilepsy, but not the underlying epileptogenesis processes, particularly in neonatal epilepsy. Newborn are more subjected to early-onset of epilepsy because of the common complications of labor in human, such as hypoxia-ischemia and pre-eclampsia. Such complications may cause major damage in the neonates’ brain, including inflammation, neuronal degeneration and other types of damage-related brain injuries. In recent years, great number of evidence point to inflammation as a potential pathway

Prenatal exposure to alcohol (ethanol) results in a continuum of physical, neurological, behavioral, and learning defects collectively grouped under the heading fetal alcohol spectrum disorders (FASD). Fetal alcohol syndrome (FAS) is the most severe combination of these defects under this heading, and is characterized by pre- and postnatal growth deficiencies, facial abnormalities, and defects of the central nervous system (CNS). The developing brain is particularly vulnerable to the toxicity of ethanol, given the broad time frame of susceptibility from neurulation, when the neural tube is formed, all the way through to birth. The cerebellum is an area of the brain particularly vulnerable to prenatal ethanol exposure. Mechanisms proposed for this drastic reduction in brain cells include apoptosis, oxidative stress, and damage to the radial glia stem cell progenitor pool. Physical dexterity, coordination, and visuospatial processing are all affected by these stressors, and eyeblink classical conditioning

As a result of these and other changes, brain mass shrinks and the brain’s inner cavity grows bigger.” This means that if a person creates an addiction for alcoholic beverages it will have a major impact on the brain cells, as it slows down neurotransmitters. Also, the continuation of consumption of this drug makes the brain not to work in an adequate way, which will later bring changes in attitude such as depression and anxiety. There can be permanent damages in the brain if the consumption is not moderate, since it affects directly parts of the brain that are essential for reasoning. Comparatively to the effect that alcohol can have on the brain, it also develops liver problems that in several cases end up bringing lethal effects.

Ethanol is the most commonly abused drug in the United States. When ethanol is ingested in small amounts, it may produce a feeling of euphoria in the body despite the fact that it is a depressant. Alcohol is a central nervous system depressant and it is the central nervous system that is most affected by the affects of alcohol. When ingested, alcohol passes from the stomach into the small intestine, where it is rapidly absorbed into the blood and distributed throughout the body. Because it is distributed so quickly and thoroughly the alcohol can affect the central nervous system even in small concentrations. Even with low concentrations, alcohol reduces inhibitions. As blood alcohol concentration increases, a person's response to stimuli decreases markedly, speech becomes slurred, and he or she becomes unsteady and has trouble walking (“Alcohol and the Human Body”).

Ethanol, the alcohol found in alcoholic beverages, has a wide range of effects. Unlike many drugs, ethanol does not have a specific area of the brain in which it exerts its effects. For this reason, ethanol has a large diversity of symptoms and varying effects among individuals. In general, it binds with and alters the function of voltage gated ion channels. Typically ethanol inhibits neurons directly or stimulates the release of inhibitor neurotransmitters. Ethanol may have undesirable side effects such as deficits in cognitive ability and long-term brain damaged if used frequently.

Notably, in congruent with our finding, NAC has been shown to provide cysteine to cells even in the absence of cysteine transport [47, 48]. Interestingly, the present finding also suggests a possibility that oxidative stress can regulate EAAC1 since NAC prevented the E-induced EAAC1 loss (Fig 7C). In support of this finding, under stressful conditions, such as oxidative and chemical stress, regulation and/or alteration of EAAC1 are evident at the level of expression, activity, and its membrane trafficking [49-52]. Clinically, NAC is the widely used Cys prodrug due to its safety, tolerability, and its ability to undergo rapid hydrolysis to deliver Cys immediately following cellular entry [46, 53, 54].

Alcohol can affect the nervous system from the immediate experience which is linked to behavioral changes. Initial alcohol consumption can impair cognition and psychomotor performance (Mumenthaler, Taylor, O 'Hara, & Yesavage, 1999) as well as decrease attention, alterations in memory, mood changes, and drowsiness (Valenzuela, 1997). Alcohol consumed by mouth is rapidly absorbed into the bloodstream from the stomach and small intestine and is able to cross the blood brain barrier (Mumenthaler, Taylor, O 'Hara, & Yesavage, 1999). These changes may be observed because alcohol affects brain function by altering its ability to properly control behavior. Alcohol can act as a depressant by increasing inhibitory neurotransmission, by decreasing excitatory neurotransmission, or through a combination of both (Valenzuela, 1997). Neurochemical effects can occur. Alcohol increases GABA activity (Suzdak, Schwartz, Skolnick, & Paul, 1986). GABA is an inhibitory neurotransmitter that is responsible for sending chemical messages through the brain and the nervous system. Therefore, as GABA activity increases, it may result in a

Alcoholic beverages have gained their popularity throughout the centuries, and has become a prominent component in the social network of the current society. However, researches have shown that alcohol consumption involves extensive risks can result in numerous diseases, including a range of birth defects and developmental disorders collectively known as the foetal alcohol spectrum disorder. This essay describes various aspects of this disease, including the definition, causes, signs and symptoms, current methods of diagnosis, as well as any treatment available and prognosis for patients with this disorder.

The effects associated with alcohol are produced by the ethanol in the alcohol. The severity of these effects is reflected by the concentration of alcohol in an individual’s blood, which is dictated by the amount of alcohol ingested, the volume of blood, the individual’s metabolism, and amount of time since ingestion. In large doses, alcohol acts as a depressant of the central nervous-system. A blood alcohol level of 0.1% affects some of the motor areas of the brain associated with speech, balance and manual dexterity. A blood alcohol level of 0.2% depresses all motor functions and the area concerned with emotions is depressed. At a blood alcohol level of 0.45% the entire section of the brain that handles perception is depressed and the individual becomes comatose. At a blood alcohol level of 0.7% the parts of the brain that control the heartbeat and breathing are depressed and the individual

It can permanently destroy your growing baby's cells, influencing how your baby's face, organs and brain develop. Heavy drinking can also damage your baby's nervous system, developing fetal alcohol spectrum disorders with issues ranging from mild learning difficulties or social problems to birth defects. Babies with fetal alcohol syndrome tend to have facial defects and smaller physiques for people their age. They also have learning difficulties, poor muscle tone and coordination, and behavioural issues, for a lifetime.

There has been a great amount of research done using the chick model to study effects of ethanol on embryonic development. It is widely accepted that ethanol-induced neural crest losses may be responsible for the craniofacial defects observed in FAS (4). It has also been shown that a critical window exists for when ethanol-induced losses will take place. Studies in mice and chicks have shown that ethanol exposure at specific stages in development results in significant cell death; however, exposure causes apoptosis in cNCCs only if it is administered before the CNN migrate into the neuroectoderm (9). Our data shows that increased ethanol concentration had a significant effect on chick head diameter, however our data did not show significant