##s Cysteine ( Cys ) And GSH?

Alcohol consumption during pregnancy can cause fetal alcohol syndrome. The severely effected victims of the syndrome have a variety of congenital defects: mental retardation, coordination problems, and heart, eye, and genitourinary malformations, as well as low birth weight and slowed growth rate. Most apparent are characteristic facial abnormalities.

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].

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

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.

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

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.

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.

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

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

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

Even a small amount of alcohol has the potential to hurt the child. The unborn child of a person who occasionally drinks is at risk of receiving fetal alcohol effects. This condition causes children to receive some of the same of the same effects that come from fetal alcohol syndrome. A child may not receive any of these conditions due to a mother’s alcohol consumption, but there are still some potential effects. Evidence shows that when a pregnant mother consumes an average of two alcoholic beverages per day, her child may have a lower amount of intelligence and is also at risk for having mental retardation. Also, there is research that suggests that even low quantities of alcohol consumed during pregnancy can have contrary effects on the child’s behavioral and psychological functions, and can cause a child to exhibit behaviors such as hyperactivity, unusual nervousness or anxiety, and poor impulse control. Alcohol consumption during pregnancy can also cause children to have less accuracy in their spatial and visual reasoning later in their lives. Due to these results, Sarah should be advised to not drink alcohol while she is

The pathophysiology of alcoholism begins after alcohol the ingestion of alcohol. It is absorbed and unaltered through the stomach and intestines. Next it is distributed throughout the body through the blood and absorbed by all tissues and fluids (Huether, 2012, p. 72). Furthermore, in the liver the alcohol blood content is metabolized into acetaldehyde by the enzymes process of alcohol dehydrogenase (ADH), the microsomal ethanol oxidizing system (MEOS), and catalase (Huether & McCance, 2012). Next, the metabolizing effects the central nervous system (CNS) and exhibits a depressant action. It is first expressed in the subcortical structures of the brain. This has an effect of disorientation of motor skills and intellect. With an increase in blood alcohol concentration, the medullary centers become depressed and as a result affects respiration (Huether & McCance, 2012). In addition, the effects of alcoholism encourage hepatic and gastric changes. The hepatic effect is caused by acetaldehyde, in which, induces inflammation, fatty deposits and enlargement of the liver (Huether & McCance, 2012).

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.

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.