Behavioral and Neuronal Effects of Inhaled Bromine Gas: Oxidative Brain Stem Damage

Autor: Samina Salim, Shama Ahmad, Aftab Ahmad, Wilson K. Rumbeiha, Nithya Mariappan, Archita Amudhan, Duha Aishah, Cristina M Santana, Iram Zafar, Shajer Manzoor, Apoorva Amudhan, Shazia Shakil, Juan Xavier Masjoan Juncos, Simmone Siddiqui
Rok vydání: 2021
Předmět:
Sympathetic nervous system
bromine
Tryptophan Hydroxylase
Rats
Sprague-Dawley
chemistry.chemical_compound
Catecholamines
Biology (General)
Neurotransmitter
Spectroscopy
Neurons
Neurotransmitter Agents
Behavior
Animal
Glial fibrillary acidic protein
biology
Chemistry
General Medicine
respiratory system
Computer Science Applications
Mental Health
medicine.anatomical_structure
Inhalation
Administration
Metabolome
Female
medicine.symptom
medicine.drug
medicine.medical_specialty
Tyrosine 3-Monooxygenase
QH301-705.5
injury
brain
Brain damage
Article
neuronal
Catalysis
Inorganic Chemistry
Dopamine
Internal medicine
Administration
Inhalation
Glial Fibrillary Acidic Protein
Genetics
halogens
medicine
Animals
Physical and Theoretical Chemistry
QD1-999
Molecular Biology
Behavior
Chemical Physics
Tyrosine hydroxylase
Animal
behavior
Organic Chemistry
Neurosciences
Tryptophan hydroxylase
Bromine
Rats
Brain Disorders
Oxidative Stress
Endocrinology
Brain Injuries
biology.protein
Catecholamine
Sprague-Dawley
Other Biological Sciences
Other Chemical Sciences
Biomarkers
Brain Stem
Zdroj: International Journal of Molecular Sciences
International journal of molecular sciences, vol 22, iss 12
International Journal of Molecular Sciences, Vol 22, Iss 6316, p 6316 (2021)
Volume 22
Issue 12
ISSN: 1422-0067
DOI: 10.3390/ijms22126316
Popis: 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.
Databáze: OpenAIRE
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