Motor activity metabolism

Effects of Metabolism on Toxicity. Whether the toxic effects seen after exposure to diisopropyl methylphosphonate are caused by the parent compound or its metabolites is unknown. Studies of IMP A show that acute-duration exposure to IMPA results in reduced motor activity, prostration, and ataxia—effects also seen after exposure to diisopropyl methylphosphonate (EPA 1992). Other studies (Little et al. 1986, 1988) show that IMPA, the major metabolite of diisopropyl methylphosphonate, has an affinity for both lung and brain tissues and will bind to proteins in these tissues—effects that were not seen after exposure to diisopropyl methylphosphonate (EPA 1992 Little et al. 1988). These data and other data on the toxicity of IMPA neither support nor contradict the data found in the diisopropyl methylphosphonate studies, so it is not possible to attribute the effects after exposure to diisopropyl methylphosphonate to IMPA. Metabolites of IMPA other than MPA have not been identified. 

The lipostat theory postulates a mechanism that inhibits eating behavior and increases energy consumption whenever body weight exceeds a certain value (the set point) the inhibition is relieved when body weight drops below the set point (Fig. 23-30). This theory predicts that a feedback signal originating in adipose tissue influences the brain centers that control eating behavior and activity (metabolic and motor). The first such factor, leptin, was discovered in 1994, and several others are now known. 

Emeretli (1990) demonstrated a convincing link between the activity of succinic dehydrogenase in the red muscle mitochondria of Black Sea species and their motor activity. This enzyme is one of the most important in the Krebs cycle, which controls the intensity of aerobic energy metabolism. 

There are also changes in the rates of metabolism as red blood cells appear and aerobic processes intensify (Lasker and Theilacker, 1962 Laurence, 1975 Timeyko and Novikov, 1991) during the early phases of ontogenesis. Oxygen consumption increases, as do the number of mitochondria and their protein contents (Abramova and Vasilyeva, 1973 Ozemyuk, 1993). The adenyl nucleotide pool (ATP and ADP) decreases (Milman and Yurovitsky, 1973 Boulekbache, 1981), while the activity of cytochrome oxidase increases (Ozemyuk, 1993). The increased energy metabolism corresponds to a considerable extent with motor activity (Reznichenko, 1980). In the yolk sac, the activity of proteinase, which supplies nitrogenous materials to the embryo, increases, as does the rate of amino acid incorporation into the body proteins. 

The population coefficients of moderately mobile, as distinct from highly mobile, Black Sea fish decrease to 1.4, and low mobile to 1, i.e. to the approximate values known for standard metabolism. These facts lend emphasis to the importance of conducting experiments in order to substantiate the conversion calculations. It is incorrect to extrapolate experimental data to total metabolism in fish without making direct observations on their motor activity in the natural state (Paloheimo and Dickie, 1966 Beamish, 1968 Brett, 1970 Healy, 1972 Elliott, 1976 Tytler, 1978 Kerr, 1982 Diana,... 

Diaz-Mayans J, Laborda R, Nunez A. 1986. Hexavalent chromium effects on motor activity and some metabolic aspects of Wistar albino rats. Comp Biochem Physiol 83C(1) 191-195. 

Repeated inhalation or oral exposures to moderate to high doses of -butyl acetate and -butanol are well tolerated. These aforementioned molecules are readily and rapidly metabolized to -butyric acid. The no-observed-effect level (NOEL) for repeated dose oral exposure to -butanol was 125 mg kg day. In a 90 day inhalation study in rats with -butyl acetate a NOEL of 500 ppm was reported for systemic effects, and a NOEL of 3000 ppm (highest dose tested) was reported for postexposure neurotoxicity based on functional observational battery endpoints, quantitative motor activity, neuropathy, and sched-uled-controlled operant behavior endpoints. Results of inhalation studies conducted on -butanol and -butyl acetate were negative for inducing reproductive and developmental toxicity. The NOEL for female reproductive toxicity was 6000 ppm with -butanol and 1500 ppm for -butyl acetate. In a 90 day repeated-dose inhalation toxicity study with butyl acetate the NOEL for male reproductive toxicity was 3000 ppm. For developmental toxicity, a NOEL of 3500 ppm was observed with -butanol and a NOEL of 1500 ppm (the highest exposure tested) was seen in both rats and rabbits following exposure to -butyl acetate. 

Mechanisms of Respiratory Control. To meet the metabolic demands of the body and to maintain the acid-base balance, ventilation is regulated by various stimuli acting at several locations in the body. Although the mechanism by which each stimulus acts in amplifying or diminishing ventilation is not well known, these stimuli clearly inhibit and excite the central respiratory centers in the medulla, either directly or indirectly. The electrical impulses generated in these centers are responsible for the motor activities which produce the ventilatory response. 

A correlation between mood and NA and A excretion by manic depressives has been reported [356]. This relationship could possibly be secondary to changes of fluid intake, water metabolism [357] or motor activity, although in a longitudinal study of a manic-depressive patient [358] it is claimed that increased excretion of DA and of NA and its metabolites during mania correlated with mood rather than with the other variables or with drug treatment. High DA excretion in mania has been confirmed [359] and seems unlikely to be simply a... 

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