Article

Central and peripheral changes in catecholamine biosynthesis and turnover in rats after a short period of ozone exposure.

Laboratoire de Physiologie Intégrative, Cellulaire et Moléculaire, UMR CNRS 5123, Bâtiment 404-Raphaël Dubois, Université Claude Bernard Lyon I, Campus de la Doua, 43 Boulevard du 11 Novembre 1918, F-69622 Villeurbanne Cedex, France.
Neurochemistry International (impact factor: 2.86). 01/2005; 45(7):979-86. DOI:10.1016/j.neuint.2004.06.015
Source: PubMed

ABSTRACT We investigated in rat the effects of ozone exposure (0.7 ppm) for 5 h on the catecholamine biosynthesis and turnover in sympathetic efferents and various brain areas. For this purpose, the activity of tyrosine hydroxylase, the rate-limiting enzyme in catecholamine biosynthesis, was assessed in superior cervical ganglia and in two major noradrenergic cell groups, A2 and A6 (locus coeruleus). Tyrosine hydroxylase activity was estimated in vivo by measuring the accumulation of l-dihydroxyphenylalanine after pharmacological blockade of L-aromatic acid decarboxylases by NSD-1015 (100 mg/kg i.p.). The catecholamine turnover rate was measured after inhibition of tyrosine hydroxylase by alpha-methyl-para-tyrosine (AMPT, 250 mg/kg, i.p., 2.5 h) in peripheral sympathetic target organ (heart and lungs) as well as in some brain catecholamine terminal areas (cerebral cortex, hypothalamus and striatum). Ozone caused differential effects according to the structure. Catecholamine biosynthesis was stimulated in superior cervical ganglia (+44%, P < 0.05) and caudal A2 subset (+126%, P < 0.01), whereas catecholamine turnover was increased in heart (+183%, P < 0.01) and cortex (+22%, P < 0.05). On the other hand, catecholamine turnover was inhibited in lungs (-53%, P < 0.05) and striatum (-24%, P < 0.05). A brief exposure to ozone, at a concentration chosen to mimic pollution level encountered in urban areas, can modulate catecholamine biosynthesis and utilization rate in the sympathetic and central neurones.

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    Journal of Epidemiology &amp Community Health 09/2005; 59(8):685-93. · 3.19 Impact Factor
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Keywords

brain catecholamine terminal areas
 
brief exposure
 
catecholamine biosynthesis
 
catecholamine turnover
 
catecholamine turnover rate
 
caudal A2 subset
 
cerebral cortex
 
differential effects
 
L-aromatic acid decarboxylases
 
major noradrenergic cell groups
 
mimic pollution level
 
modulate catecholamine biosynthesis
 
ozone exposure
 
rate-limiting enzyme
 
superior cervical ganglia
 
sympathetic efferents
 
tyrosine hydroxylase
 
Tyrosine hydroxylase activity
 
urban areas
 
utilization rate