Decreasing synthesis

After the extraction of lipid and nonlipid components from the leaves of mandarin orange Citrus reticulata, the lipid fraction was further separated by PTLC to determine different lipid classes that affect the chemical deterrence of C. reticulata to the leaf cutting ecat Acromyrmex octopinosus. These lipids seem to be less attractive to the ants [81a]. The metabolism of palmitate in the peripheral nerves of normal and Trembler mice was studied, and the polar lipid fraction purified by PTLC was used to determine the fatty acid composition. It was found that the fatty acid composition of the polar fraction was abnormal, correlating with the decreased overall palmitate elongation and severely decreased synthesis of saturated long-chain fatty acids (in mutant nerves) [81b]. 

Hypersensitivity reactions (fever, hypotension, rash, dyspnea in 25%), much lower risk with polyethylene gycol form low emetogenic potential pancreatitis decreased synthesis of proteins, clotting factors CNS lethargy... 

The answer is d, (Hardman, p 617. Katzung, p 318.) Most NSAlDs inhibit both cyclooxygenase I and II, resulting in decreased synthesis of prostaglandins, prostacyclins, and thromboxanes. 

In brain, as in most mammalian cells, thiamine occurs predominantly in the form of TDP, the remainder being made up of thiamine monophosphate (10%), thiamine triphosphate (5-10%) and trace amounts of free thiamine. Thiamine is transported into brain and phosphory-lated by the action of thiamine pyrophosphokinase, and inhibition of this enzyme by thiamine antagonists such as pyrithiamine results in decrease synthesis of TDP. Treatment of experimental animals with pyrithiamine results in a generalized reduction of TDP concentrations and an early selective loss in activity of a-KGDH in regions... 

Nonselective NSAIDs (including aspirin) cause gastric mucosal damage by two mechanisms (1) a direct or topical irritation of the gastric epithelium, and (2) systemic inhibition of the cyclooxygenase-1 (COX-1) enzyme, which results in decreased synthesis of protective prostaglandins. 

Anhaptoglobinemia or subnormal Hp values, often found in acute and chronic liver disease, and in mononucleosis, may also be caused by an increased consumption and not by decreased synthesis. In both disorders there exists a tendency for the development of splenomegaly, i.e., a tendency to retarded splenic blood flow with slightly shortened survival time of the red cells as a consequence. If we do not presume a half-life of Hp in normals below one day, the main part of the Hp catabolism must be secondary to Hb release. Hence, subnormal Hp values will probably appear in conditions with no clinically observable increased hemolysis or slightly decreased Hp synthesis. The latter may be a con-... 

Loss of muscle protein in trauma is caused by increased degradation rather than decreased synthesis. The degradation is controlled by changes in the levels of glucocorticoids, insulin and the proinflammatory cytokines TNFa and IL-1. The proteolytic enzyme complex that degrades the protein is the proteasome (Chapter 8). The mechanism by which the enzyme is activated is not known, but increased activities of the enzymes involved in ubiquitina-tion of proteins and an increase concentration of ubiquitin may play a role (Chapter 8). 

Dietary supplementation with Tyris necessary to make up for decreased synthesis. 

Smyth et al. 1936). In some cases, moderate elevations in white cell counts are observed, perhaps in response to necrosis in the liver or kidneys. In a few cases, mild anemia is observed (Gray 1947), and occasionally this may become severe (Straus 1954). The mechanism underlying the blood dyscrasia is not known, but anemia might be secondary to internal hemorrhaging as a result of decreased synthesis of clotting factors by the liver (Guild et al. 1958 Stevens and Forster 1953 Straus 1954). 

Cyclosporine can bind to the cytosolic protein cy-tophilin C. This drug-protein complex inhibits cal-cineurin phosphatase activity, which leads to a decreased synthesis and release of several cytokines, including interleukins IL-2, IL-3, IL-4, interferon-a, and tumor necrosis factor. 

Control of androgen secretion and activity and some sites of action of antiandrogens (1), competitive inhibition of GnRH receptors (2), stimulation (+, pulsatile administration) or inhibition via desensitization of GnRH receptors (-, continuous administration) (3), decreased synthesis of testosterone in the testis (4), decreased synthesis of dihydrotestosterone by inhibition of 5a-reductase (5), competition for binding to cytosol androgen receptors. 

Factors that alter the level of testosterone, by decreasing synthesis, increasing metabolic clearance or blocking the androgen receptor, can adversely affect the amount or quality of semen. It has been reported that exposure to environmental chemicals may lead to reduced semen quality (see chapter 4). 

A deficiency in dihydrobiopterin reductase or dihydrobioptenn synthetase leads to hyperphenylalaninemia, and decreased synthesis of catecholamines and serotonin. 

Increased ALA synthase activity One common feature of the j porphyrias is a decreased synthesis of heme. In the liver, heme normally functions as a repressor of ALA synthase. Therefore, Ihe absence of this end product results in an increase in the synthesis of ALA synthase (derepression). This causes an increased syn thesis of intermediates that occur prior to the genetic block. The accumulation of these toxic intermediates is the major pathophysi ology of the porphyrias. 

The ethanol-mediated increase in NADH causes 1 the intermediates of gluconeogenesis to be diverted into alternate reaction pathways, resulting in decreased synthesis of glucose. 

VLDL in the plasma is converted to LDL—a much smaller, denser particle. Apo CM and apo E are returned to HDLs, but the LDL retains apo B-100, which is recognized by receptors on peripheral tissues and the liver. LDLs undergo receptor-mediated endocytosis, and their contents are degraded in the lysosomes. A deficiency of functional LDL receptors causes type II hyperlipidemia (familial hypercholesterolemia). The endocytosed cholesterol inhibits HMG CoA reductase and decreases synthesis of LDL receptors. Some of it can also be esterified by acyl CoAxholesterol acyltransferase and stored. 

Definition of porphyrias, their modes of genetic inheritance, and their treatment Porphyrias are caused by inherited (or occasionally acquired) defects in heme synthesis, resulting in the accumulation and increased excretion of porphyrins or porphyrin precursors. Porphyrias are classified as erythropoietic or hepatic, depending where the enzyme deficiency occurs. With the exception of congenital erythropoietic porphyria, which is a genetically recessive disease, all the porphyrias are inherited as autosomal dominant disorders. All porphyrias result in a decreased synthesis of heme and, therefore, ALA synthase is dere-pressed. The severity of symptoms of the porphyrias can be diminished by intravenous injections of hemin. Because some porphyrias result in photosensitivity, avoidance of sunlight is helpful. 

Pernicious anemia is usually caused by poor absorption of the vitamin. Absorption depends upon the intrinsic factor, a mucoprotein (or rnuco-proteins) synthesized by the stomach lining.ad 1 Pernicious anemia patients often have a genetic predilection toward decreased synthesis of the intrinsic factor. Gastrectomy, which decreases synthesis of the intrinsic factor, or infection with fish tapeworms, which compete for available vitamin B12 and interfere with absorption, can also induce the disease. Also essential are a plasma membrane receptors 1 and two blood transport proteins... 

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