Abstract
The risk of accidental bromine (Br2) exposure to the public has increased due to its enhanced industrial use. Inhaled Br2 damages the lungs and the heart; however, adverse effects on the brain are unknown. In this study, we examined the neurological effects of inhaled Br2 in Sprague Dawley rats. Rats were exposed to Br2 (600 ppm for 45 min) and transferred to room air and cage behavior, and levels of glial fibrillary acidic protein (GFAP) in plasma were examined at various time intervals. Bromine exposure resulted in abnormal cage behavior such as head hitting, biting and aggression, hypervigilance, and hyperactivity. An increase in plasma GFAP and brain 4-hydroxynonenal (4-HNE) content also was observed in the exposed animals. Acute and delayed sympathetic nervous system activation was also evaluated by assessing the expression of catecholamine biosynthesizing enzymes, tryptophan hydroxylase (TrpH1 and TrpH2), and tyrosine hydroxylase (TyrH), along with an assessment of catecholamines and their metabolites. TyrH was found to be increased in a time-dependent manner. TrpH1 and TrpH2 were significantly decreased upon Br2 exposure in the brainstem. The neurotransmitter content evaluation indicated an increase in 5-HT and dopamine at early timepoints after exposure; however, other metabolites were not significantly altered. Taken together, our results predict brain damage and autonomic dysfunction upon Br2 exposure.
Highlights
Bromine (Br2 ) is a volatile brownish-yellow fuming liquid
Our results demonstrated that these rats had significant increases in glial fibrillary acidic protein (GFAP) in plasma and
A trend towards an increase in Homovanillic acid (HVA), which is a marker for metabolic stress, was observed after bromine exposure [19]
Summary
Bromine (Br2 ) is a volatile brownish-yellow fuming liquid. It has a strong pungent and suffocating odor that is irritating to the nasal mucosa. We have demonstrated the occurrence of brominated fatty acids and fatty aldehydes, in the tissues of Br2 -exposed animals, that form upon reaction of Br2 with pulmonary plasmalogens [2,5] These circulate in the blood and are transported to other major organs in the body long after exposure [1]. Our studies have shown that a single dose of acute Br2 exposure causes decreased heart rate, cardiac hypertrophy, increase in cardiac injury markers in blood, and increased ultrastructural damage [1,2]. We demonstrated that this SERCA inactivation was accompanied by increased cytosolic calcium (Ca2+ ) overload and increased Ca2+ -sensitive LV protease (calpain) activity These effects were followed by our group in the Br2 -exposed rats for prolonged durations to observe the delayed effects. We evaluated the brainstem as it contains the regions that control the respiratory center
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