Monoamine oxidase activated

Vanadium. Vanadium is essential in rats and chicks (85,156). Estimated human intake is less than 4 mg/d. In animals, deficiency results in impaired growth, reproduction, and Hpid metaboHsm (157), and altered thyroid peroxidase activities (112). The levels of coen2yme A and coen2yme Q q in rats are reduced and monoamine oxidase activity is increased when rats are given excess vanadium (157). Vanadium may play a role in the regulation of (NaK)—ATPase, phosphoryl transferases, adenylate cyclase, and protein kinases (112). 

Chakrabarti SK, Loua KM, Bai C, Durham H, Panisset JC. 1998. Modulation of monoamine oxidase activity in different brain regions and platelets following exposure of rats to methyhnercury. Neurotoxicol Teratol 20 161-168. 

Marker, H.S., Weiss, C., Silides, D.J., and Cohen, G. (1981). Coupling of dopamine oxidation (monoamine oxidase activity) to glutathione oxidation via the generation of hydrogen peroxide in rat brain homogenates. J. Neurochem. 36, 589-593. 

Davis BA, Yu PH, Carlson K, O Sullivan K, Boulton AA. 1982. Plasma levels of phenylacetic acid, m- and p-hydroxy-phenylacetic acid, and platelet monoamine oxidase activity in schizophrenic and other patients. Psychiatry Res 6 97. de la Torre R, Ortuno J, Pascual JA, Gonzalez, S, BaUesta J.1998. Quantitative determination of tricyclic... 

MPTP-induced toxicity and monoamine oxidase activity in the mouse brain. 

Soliman. Eood constituents attenuate monoamine oxidase activity and peroxidase levels in G6 astrocyte cells. 

Reversible inhibitor of monoamine oxidase activity (RIMA). (Atypical agent. 

Carrasco, J. L., J. Saiz-Ruiz, E. Hollander, J. Cesar, and J. J. Lopez-Ibor. 1994. "Low Platelet Monoamine Oxidase Activity in Pathological Gambling." Acta Physiologica Scandinavica 90 427-31. 

Fowler, C. J., L. von Knorring, and L. Oreland. 1980. "Platelet Monoamine Oxidase Activity in Sensation Seekers." Psychiatry Research 3 273-79. 

Many of the biochemical processes that generate chemical energy for the cell take place in the mitochondria. These organelles contain the biochemical equipment necessary for fatty acid oxidation, di- and tricarboxylic acid oxidation, amino acid oxidation, electron transport, and ATP generation. In this experiment, a mitochondrial fraction will be isolated from beef heart muscle. The mitochondria will be analyzed for protein content and fractionated into submitochondrial particles. Each fraction will be analyzed for malate dehydrogenase and monoamine oxidase activities. 

The numbers represent the % total activity. For example, 82% of the total monoamine oxidase activity of mitochondria is found In the outer membrane. 

Students will isolate intact mitochondria from beef heart and fractionate them to prepare submitochondrial particles. Each fraction will be characterized by protein estimation by the biuret method and measurement of malate dehydrogenase and monoamine oxidase activity. 

Nimmo-Smith, R.H. and Raison, C.G. (1968) Monoamine oxidase activity of Schistosoma mansoni. Comparative Biochemistry and Physiology C 62, 403—416. 

At high concentrations, phenytoin also inhibits the release of serotonin and norepinephrine, promotes the uptake of dopamine, and inhibits monoamine oxidase activity. The drug interacts with membrane lipids this binding might promote the stabilization of the membrane. In addition, phenytoin paradoxically causes excitation in some cerebral neurons. A reduction of calcium permeability, with inhibition of calcium influx across the cell membrane, may explain the ability of phenytoin to inhibit a variety of calcium-induced secretory processes, including release of hormones and neurotransmitters. The significance of these biochemical actions and their relationship to phenytoin s clinical activity are unclear. 

Dehouck MP, Meresse S, Delorme P et al. (1990) An easier, reproducible, and mass-production method to study the blood-brain barrier in vitro. J Neurochem 54 1798-1801 Meresse S, Dehouck MP, Delorme P et al. (1989) Bovine brain endothelial cehs express tight junctions and monoamine oxidase activity in long-term culture. J Neurochem 53 1363-1371... 

Linezolid inhibits monoamine oxidase activity and has been reported to cause serotonin toxicity in combination with paroxetine. While some patients have apparently taken the combination of linezolid and an SSRI safely, this report suggests that patients taking combined treatment should be monitored for serotonin toxicity. 

Figure 9.18 shows a representative chromatogram of the substrates and products of liver monoamine oxidase activity. Figure 9.19 illustrates results with phenol sulfotransferase activity. 

Figure 9.18 Chromatograms of the substrates and products of liver monoamine oxidase activity. Upper tracing a, dopamine, b, Dopac. Lower tracing a tyramine, b, Hopac. The retention time for dopamine, Dopac, tyramine, and Hopac was 4.0,7.0, 6.0, and 10.7 minutes, respectively. (From Sim and Hsu, 1990.)...

Kalaria RN, Mitchell MJ, Harik SI (1987) Correlation of l-methyl-4-phenyl-1,2,3,6- tetrahydropyridine neurotoxicity with blood-brain barrier monoamine oxidase activity. Proc Natl Acad Sci USA 84 3521-3525. 

Diethylamine is a primary skin irritant and is an irritant to the eyes and mucous membranes. The dermal LD50 in rabbits was 580mgkg . An inhalation LC50 of 4000ppm in rats was reported for a 4h exposure. The oral LD50 in rats has been reported to be 540 mg kg Intraperitoneal injection in rats resulted in a moderate inhibitory effect with respect to liver function and monoamine oxidase activity. 

PPA has been demonstrated to competitively and reversibly inhibit monoamine oxidase activity in both human brain and rat liver. 

Development and growth - Brain HT is lower in fetal and newborn rats than in the adult and increases in extrauterine life, as do the catecholamines l. At birth monoamine oxidase activity is low but the decarboxylase is as active as in the mature rat. The low levels of HT probably result from low activity of the enzyme that hydroxylates TP82, 83. Also in rabbits and chicks, brain HT increases during fetal and early postnatal life, but results on guinea pigs conflict S, 86. 

Somewhat different results were reported from other laboratories n-3 fatty acid deficiency in rats caused a decrease in dopamine level and D2-receptor density in the frontal cortex as well as a decrease in serotonin receptor density (Delion, 1994,1996), whereas fish oil increased the dopamine level (Chalon, 1998). A decrease in the dopamine release from the frontal cortex was also detected by the microdialysis method after thyramine stimulation but not after KCl stimulation (Zimmer, 1998, 2000). In aged rats, however, the monoamine level was not affected, whereas monoamine oxidase activity was decreased during n-3 fatty acid deficiency (Delion, 1997). 

---