In vivo oxidation

In most cases, ketonemia is due to increased production of ketone bodies by the liver rather than to a deficiency in their utilization by extrahepatic tissues. While acetoacetate and d(—)-3-hydroxybutyrate are readily oxidized by extrahepatic tissues, acetone is difficult to oxidize in vivo and to a large extent is volatilized in the lungs. 

Bogan L, RT Lamar, KE Hammel (1996) Fluorene oxidation in vivo by Phanerochaete chrysosporium and in vitro during manganese peroxidase-dependent lipid peroxidation. Appl Environ Microbiol 62 1788-1792. 

However, peroxidation can also occur in extracellular lipid transport proteins, such as low-density lipoprotein (LDL), that are protected from oxidation only by antioxidants present in the lipoprotein itself or the exttacellular environment of the artery wall. It appeats that these antioxidants are not always adequate to protect LDL from oxidation in vivo, and extensive lipid peroxidation can occur in the artery wall and contribute to the pathogenesis of atherosclerosis (Palinski et al., 1989 Ester-bauer et al., 1990, 1993 Yla-Herttuala et al., 1990 Salonen et al., 1992). Once initiation occurs the formation of the peroxyl radical results in a chain reaction, which, in effect, greatly amplifies the severity of the initial oxidative insult. In this situation it is likely that the peroxidation reaction can proceed unchecked resulting in the formation of toxic lipid decomposition products such as aldehydes and the F2 isoprostanes (Esterbauer et al., 1991 Morrow et al., 1990). In support of this hypothesis, cytotoxic aldehydes such as 4-... 

Penicillamine reacts with pyridoxal-5-phosphate to form a thiazolidine derivative, and is able to displace many amino acids from their Schiff base complexes, forming stable compounds of this type. The reactivity of the thiol group of penicillamine is less than that of cysteine, probably because of steric hindrance by the adjacent methyl groups of penicillamine, which in consequence is less rapidly oxidized in vivo [7]. 

D.Z. Levine, K.D. Bums, J. Jaffey, and M. Iacovitti, Short-term modulation of distal tubule fluid nitric oxide in vivo by loop NaCl reabsorption. Kidney Int. 65, 184—189 (2004). 

It has been already pointed out that nitric oxide exhibits antioxidant effect in LDL oxidation at the NO/ 02 ratio 1. Under these conditions the antioxidant effect of NO prevails on the prooxidant effect of peroxynitrite. Although some earlier studies suggested the possibility of NO-mediated LDL oxidation [152,153], these findings were not confirmed [154]. On the other hand, at lower values of N0/02 ratio the formed peroxynitrite becomes an efficient initiator of LDL modification. Beckman et al. [155] suggested that peroxynitrite rapidly reacts with tyrosine residues to form 3-nitrotyrosine. Later on, Leeuwenburgh et al. [156] found that 3-nitrotyrosine was formed in the reaction of peroxynitrite with LDL. The level of 3-nitrotyrosine sharply differed for healthy subjects and patients with cardiovascular diseases LDL isolated from the plasma of healthy subjects contained a very low level of 3-nitrotyrosine (9 + 7 pmol/mol 1 of tyrosine), while LDL isolated from aortic atherosclerotic intima had a 90-fold higher level (840 + 140 pmol/moD1 of tyrosine). It has been proposed that peroxynitrite formed in the human artery wall is able to promote LDL oxidation in vivo. 

Inorganic arsenicals are oxidized in vivo, biomethylated, and usually excreted rapidly in the urine, but organoarsenicals are usually not subject to similar transformations. 

Octamethylpyrophosphoramide is also enzymicahy oxidized in vivo, as well as chemically by permanganate, to a highly effective anti-esterase.5... 

Memon, R.A., Staprans, L, Noor, M., Hoheran, W.M., Uchida, Y., Moser, A.H., Granfeld, and C. Feingold, K.R., 2000, Infection and inflammation induce LDL oxidation in vivo, Arterioscler. Thromb. Vase. Biol.20 1536-1542. 

Benzene has a low threshold limit value or TLV. The time weighted average TLV (TWA) is the allowable exposure for an average 8 hr day or a 40 hr week. The short-term exposure limit TLV (STEL) is the maximum allowable exposure for any 15-min period. For benzene the TWA = 0.5 ppm and the STEL is 2.5 ppm, as given by the American Conference of Governmental Industrial Hygienists (ACGIH). This allowable exposure is much lower than those for toluene and xylene, probably because these latter two compounds have benzyl ic positions that are easily oxidized in vivo to compounds that can be eliminated from the body. 

There is some evidence suggesting that camosine can upregulate immune function. Camosine s ability to react with hypochlorite anions (Formazyuk et al, 1992 Quinn et al, 1992) generated in activated leukocytes via the myeloperoxidase reaction, suggests that the dipeptide may limit hypochlori te-med ia ted oxidation in vivo (Pattison and Davies, 2006)... 

The synthetic form is the alcohol, panthenol, which can be oxidized in vivo to pantothenic acid. It is included in the list of substances that may be added in foods and in food supplements [403], Pantothenic acid is part of the coenzyme A (CoA) molecule therefore it is involved in acylation reactions, such as in fatty acid and carbohydrate metabolism. 

Adrenaline and noradrenaline are unstable in aqueous solution where they are subjected to spontaneous oxidation. In vivo this mechanism is only relevant under pathophysiological conditions of an catecholamine excess, since two enzymes, the catechol-O-methyltransferase (COMT) and the monoamineoxidase (MAO), inactivate physiological amounts of the transmitters. There are at least two subtypes of the enzyme MAO, A and B, which can be inhibited selectively for therapeutic purposes, for example by moclobemide and selegiline. 

When male F-344 rats were injected with NNN-2 -14c, 75-95% of the dose was excreted in the 48 hr urine. In one experiment, the urine was collected in vessels containing DNP reagent. However, the DNPs of 4-hydroxy-l-(3-pyridyl)-l-butanone and 4-hy-droxy-4-C3-pyridy1)butanal were not detected. Since this was likely due to further oxidation in vivo, methods were developed for isolation of their probable oxidation products. This resulted in identification of the lactone, 5- C3-pyridyl)—tetrahydrofuran-2-one (1-2%), the keto acid, 4-(3-pyridyl).-4-oxobutyric acid (1-2%) and the hydroxy acid, 4-(3-pyridyl)-4-hydroxybutyric acid (26-40%) as urinary metabolites. These metabolites resulted. 

A phenolic 4 -OH group, which may be generated metabolically (e.g., by oxidation in vivo) if originally absent. 

The second reaction and certainly the major route for the destruction of nitric oxide in vivo is the fast and irreversible reaction with oxyhemoglobin (Hb) or oxymyoglobin to produce nitrate. 

Although nitric oxide has an unpaired electron, it is difficult to detect directly by electron paramagnetic resonance. In addition to the low concenttation of nitric oxide in vivo, the angular momentum of the unpaired electron can couple with the angular momentum of the nitric oxide molecule to obscure the paramagnetic properties of nitric oxide (Jones, 1973). However, nitric oxide can be detected as a complex with heme groups, which has been used to show the... 

Arsine gas is oxidized in vivo and exerts a potent hemolytic effect associated with alteration of ion flux across the... 

Such a mechanism might play an important role in a metal-ion-catalyzed enzymic oxidation in vivo, in which metal ions work cooperatively 166. A synchronous four-electron-transfer requires a specific spatial arrangement which should be posable in a macromolecular environment. 

LDL becomes oxidized in vivo. There is evidence that LDL is protected against oxidation in plasma by water-soluble antioxidative substances, such as ascorbic acid, uric acid, or bilirubin. Thus, it is likely that the majority of oxidative modification of LDL occurs in the artery wall, where LDL is largely isolated from the plasmatic antioxidants. Recent evidence suggests that metal ions (copper or iron) and the enzymes myeloperoxidase and lipoxygenase play major parts in the modification of LDL [161]. 

Elemental mercury is oxidized in vivo to inorganic mercury, a bio transformation that is probably catalyzed by catalase. It is selectively accumulated in the kidney and also by lysosomes. Inorganic mercury (Hg2+) will induce the synthesis of metallothionein. Mercury binds to cellular components such as enzymes in various organelles, especially to proteins containing sulfydryl groups. Thus, in the liver, cysteine and GSH will react with mercury to produce soluble products, which can be secreted into the bile or blood. 

To determine the influence of chlorogenic acids on various stage of lipid free radical oxidation in vivo and in vitro, it is necessary to use a highly sensitivity method, such as the chemiluminescence method. 

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