The first step is where the substrate enters the active site on the enzyme. It is held there by hydrophobic interactions between the exposed non-polar groups of the enzyme residues and the side chain of the substrate. The second step is where the hydroxyl group on Serine 195, aided by the histidine-serine hydrogen bonding, preforms its nucleophilic attack on the carbonyl carbon of an aromatic amino acid. While this happens, it also transfers the hydroxyl hydrogen to the histidine nitrogen. The nucleophilic attack pushes the carbonyl electrons onto the carbonyl oxygen, which forms a short-lived intermediate.
Throughout the urea cycle, the amino acid, arginine, is changes into ornithine- this is another amino acid when hydrated, that is when water was added. During this reaction, urea is the product formed (Nelson and Cox 2008). Figure 1 shows the urea cycle, occurs specifically in the mitochondria and cytosol in the liver. (Nelson and M.Cox 2008). Urea is made in the liver by means of enzymes in the urea cycle.
Enzymes are proteins that significantly speed up the rate of chemical reactions that take place within cells. Some enzymes help to break large molecules into smaller pieces that are more easily absorbed by the body. Other enzymes help bind two molecules together to produce a new molecule. Enzymes are selective catalysts, meaning that each enzyme only speeds up a specific reaction. The molecules that an enzyme works with are called substrates.
INTRODUCTION Antibiotic as is any chemical or drug that can be used to effectively either halt the growth of, destroy toxins from or destroy the entire organism. They are said to be narrow or wide/extended in their range of activity depending on if they act on a limited number of organisms or a vast number of organisms respectively. Antibiotics resistance occurs when a microbe or a group of microbes develop a mechanism to reduce the potency or efficacy of a drug which was once effective as its treatment.  Most antibiotics in the market today usually target an exclusive biology of an organism in such a way that the drug will affect the organism specifically and do little or no harm to the host, so in any event an organism mutates genes coding
INTRODUCTION Carbon tetrachloride (CCl4) - an organic industrial solvent used in industry – is a vigorous carcinogenic agent that may create dysfunction of lung, liver, kidney and nervous system (1, 2). After being absorbed from gastrointestinal system, respiratory system and skin CCl4 is metabolized by cytochrome P-450 and exerts its toxic effects via its metabolites trichloromethyl free radical and trichloromethyl peroxyl radical (1-3). These free radicals interacts with fatty acids of lung cell membrane and increase lipid peroxidation and DNA fragmentation. Moreover, they suppress antioxidant enzymes including catalase, superoxide dismutase, glutathione (GSH), oxidized glutathione (GSSG), glutathione reductase and glutathione peroxide (1,2,4).
The results are expressed as endotoxin units (EU), which is a measure of endotoxin potency rather than the quantity. This reflects the variability in toxicity of naturally occurring LPS (rapidmicrobiology n.d.). The chromogenic method uses a synthetic substrate that brings about a colour change when it is cleaved by endotoxin-activated protease. The turbidimetric method on the other hand, relies on the a coagulin gel cot forming which will alter the turbidity of the sample. Both the turbidimetric and the chromogenic methods can be used as quantitative kinetic methods simply by plotting standard curves of time vs endotoxin concentration.
This leads to lipid peroxidation and oxidative DNA loss but can interfere with physiology and intracellular signal transduction. The resulting change in intracellular redox status leads to the activation of protein kinase, for example, tyrosine kinase, protein kinase c, and the mario-activated protein kinase cascade leading to modified cellular functions. Oxidative stress compounds hypothyroidism. Hypothyroidism is a state that increases the oxidative stress. In this study, the biomarker is high in MDA level therapy-innocent primary hypothyroid patients.
It also increases lymphocyte production and T- and Bcell activity (Fuller et al., 1992; Grob et al., 1996; Maxwell et al., 1995; Noonan et al., 1996). By modulating immune defense, beta-carotene might have an impact on carcinogenesis. In addition, beta-carotene may modulate skin carcinogenesis by a reduction of lipid peroxidation in human skin, either as a free radical scavenger or as specific lipoxygenase inhibitor. The substrates of lipoxygenasesare linoleic acid and arachidonic acid; the reaction produces leukotrienes, lipoxins, and physiologically active oxygenated fatty acids. Linoleic acid is one of the major components of membrane phospholipids of living cells that are damaged by reactive oxygen species, leading to pathological events and aging processes.
Fusion helps to reduce stress by adding the contents of somewhat damaged mitochondria as a form of complementation . Fusion of the mitochondria is brought about by the process of 3 dynamin-related GTPases which are mitofusin 1 and mitofusin 2 which are both on the outer membrane and also by the optic atrophy on the inner mitochondrial membrane. One of the functions of fission is to create new mitochondria and to control the quality of the mitochondria by facilitating apoptosis during situations of high levels of cell stress and also by removing damaged mitochondria that remain in the cell. Fission is brought about by dynamin-related protein 1 . Fusin and fission play important roles when it comes to mitochondrial diseases and defects.
Cycloheximide applies its impact by interfering with the translocation steps in protein synthesize (development of two tRNA atoms and mRNA in connection to the ribosome), hence blocking translational prolongation. Cycloheximide is generally utilized as a part of biomedical research to repress protein synthesize in eukaryotic cells except for S.aureus and E.coli contemplated in vitro (i.e. outside of microorganism). It is cheap and works quickly. Actually after the interaction of 72 hours, both growth of E.coli and S.aureus will be inhibited by Cycloheximide antibiotic.