Caffeine Term Paper

Caffeine is a compound that has a molecular formula of C8H10N4O2 and is commonly known as methylxanthine [1]. The systemic name of caffeine is either 3,7-dihydro-1,3,7-trimethyl-1H-purine-2,6-dione or 1,3,7-trimethyl xanthine. Other names that are used to refer to caffeine include mateine, theine, coffeine, and guaranine. It is a chiral molecule and has no stereoisomers. The caffeine compound has two groups of amide that predominantly exist as zwitterionic resonance structures. In these structures, the atoms of nitrogen and carbon are bonded through a double bond to one another making the two nitrogen atoms are basically planar. This results in a fused ring system that has ten pi electrons in total and thus the molecule is said to be aromatic according to the Hückel's rule.
The production of caffeine occurs naturally in a number of plants including tea, coffee beans and guarana [1]. The synthesis of caffeine in plants takes place using starting materials that are purine nucleotides like GMP, AMP, and IMP and are changed into xanthosine. Xanthosine is then changed to form theobromine, which is the penultimate caffeine precursor. The pathway of the synthesis of caffeine starts from xanthosine as shown in figure 1. The synthesis involves activity of three N-methyltransferases that are SAM-dependent. These enzymes are 7-methylxanthine N-methyltransferase, xanthosine N-methyltransferase, and theobromine N-methyltransferase. 7-methylxanthosine synthase that is found in coffee has a specific xanthosine N-methyltransferase activity and is involved in the conversion of xanthosine to form 7-methylxanthosine.
Figure 1: Caffeine synthesis pathway [2]
A pure compound of caffeine is usually white in color and has a melting point of around 228OC. The solubility of caffeine is moderate in water with a temperature that equal to the room temperature. However, the solubility of caffeine in boiling water is very high. It also has a moderate solubility in ethanol. The caffeine is weakly basic with a pKa of about 0.6 and needs a very strong acid for it to be protonated.
Caffeine occurs in varying amounts in the leaves, seeds, as well as fruit of a number of plants, where it serves as a natural pesticide, which paralyzes and leads to death of some insects that feed on the plants, as well as increasing the memory of pollinators reward. It is most normally utilized by humans in extracts derived from the coffee plant seed and the tea bush leaves, as well as from a variety of foods and drinks that contain products extracted from the kola nut [3].
Caffeine causes effects on sleep, although it affects different people in different ways. It ameliorates performance in the course of deprivation of sleep but may result in successive insomnia [4]. In shift laborers, it results in less mistakes that arise from tiredness. In sports, moderate caffeine doses can enhance endurance, sprint, as well as team performance, but the meliorations are usually not very large [5].
Intake of large quantities of caffeine may lead to a condition referred to as caffeinism that combines dependency on caffeine with a broad range of unpleasant mental and physical conditions that include irritability, nervousness, insomnia, restlessness, heart palpitations, and headaches following use of caffeine [6].
Within the body caffeine serves through a number of mechanisms, but its most vital effect is to offset a substance known as adenosine, which circulates naturally at high degrees all over the body, and particularly in the nervous system. In the brain, adenosine serves a usually defensive function, part of which is to decrease levels of neural activity, for instance, there is a number of proof that adenosine aids in inducing torpor in animals that hibernate seasonally [7].
Adenosine serves as an inhibitor neurotransmitter, which causes suppression of activity in the central nervous system. Intake of caffeine counteracts adenosine and raises activity in neurotransmission that include epinephrine, acetylcholine, serotonin, dopamine, glutamate, cortisol, norepinephrine, and in higher dosages, endorphins that give the explanation of the anodyne effect to a number of users. At very high dosages, beyond 500 milligrams, caffeine suppresses neurotransmission of GABA. This proof offers an explanation as to why caffeine leads to insomnia, anxiety, rapid heart as well as respiration rate. Since caffeine is both lipid-soluble and water-soluble, it readily passes over the blood–brain barrier that divides the bloodstream from the inner parts of the brain. While in the brain, the main form of action is as a nonselective adenosine receptors antagonist, an agent that decreases the consequences of adenosine. The molecule of caffeine is similar in structure to adenosine, and has the capability to bind to receptors of adenosine on the surface of cells with no need to activate them, thus serving as a competitive inhibitor [8].
Adenosine is usually found in all parts of the body since it serves a function in the basic adenosine triphosphate, ATP, related mechanism of energy production and is also required for synthesis of RNA, but it has extra roles in the brain. The proof shows that adenosine in the brain serves to defend the brain through suppression of neural activity as well as through raising flow of blood via receptors situated on vascular smooth muscle [9]. Levels of brain adenosine are raised by diverse types of metabolic pressure that include deficiency of oxygen, as well as disruption of flow of blood. There is proof that adenosine serves as a synaptically released neurotransmitter in various components of the brain. However, adenosine increases that are associated with stress seem to be released mainly by ATP extracellular metabolism. Different from the majority of neurotransmitters, adenosine does not appear to be packaged into vesicles, which are produced in a voltage-monitored way, but the likelihood of such a mechanism has not been fully eliminated [9].
Various adenosine receptors’ categories have been depicted, with dissimilar anatomical distributions. A1 receptors are broadly disseminated, and serve as an inhibitor of uptake of calcium. There is a heavy concentration of A2A receptors in the basal ganglia, a part that plays a vital role in control of behavior, although can be present in other components of the brain also, in lower concentrations. There is proof that A 2A receptors interrelate with the system of dopamine that is engaged in arousal as well as reward. A2A receptors may as well be present on walls of arteries as well as cell membranes of blood [10].
Outside its general effects of neuroprotection, there are grounds to consider that adenosine might be more specially engaged in control of the cycle of sleep-wake. In a research by Robert McCarley together with his co-workers have reasoned that accretion of adenosine might be a main root of the sensation of sleepiness, which comes after lengthy mental activity and that the results might be mediated both through suppression of wake-enhancing neurons through A1 receptors, as well as activation of sleep-enhancing neurons through indirect consequences on A2A receptors [10]. Additional research studies have offered extra proof for the significance of A2A, but not A1, receptors.
Caffeine, just like other xanthines, also serves as an inhibitor of phosphodiesterase. Several possible mechanisms have been suggested for the performance-promoting consequences of caffeine in athletics [11]. In the metabolic or classic theory, caffeine might raise utilization of fat and reduce utilization of glycogen. Caffeine causes mobilization of free fatty acids from fat and intramuscular triglycerides through raising levels of circulating epinephrine. The raised accessibility of free fatty acids raises oxidation of fat and saves glycogen of muscles, thus heightening endurance functioning. In the nervous system, caffeine might decrease the perceptual experience of effort through reducing the activation threshold of neuron, rendering it easier to employ the muscles for work out [12].
In conclusion, the caffeine is a compound that can be produced from many plants and is usually synthesized from purine nucleotides. The small size of caffeine enables it to pass the barrier that divides the brain and the blood where it works as an antagonist of the receptors of adenosine. There has been no major regulations against caffeine as there rate of addiction is low.
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