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

• Published in: International journal of molecular sciences 2021-06, Vol.22 (12), p.6316
• Main Authors: Shakil, Shazia, Masjoan Juncos, Juan Xavier, Mariappan, Nithya, Zafar, Iram, Amudhan, Apoorva, Amudhan, Archita, Aishah, Duha, Siddiqui, Simmone, Manzoor, Shajer, Santana, Cristina M, Rumbeiha, Wilson K, Salim, Samina, Ahmad, Aftab, Ahmad, Shama
• Format: Article
• Language: English
• Subjects: 4-Hydroxynonenal; Administration, Inhalation; Aggressiveness; Animals; Apoptosis; Autonomic nervous system; Behavior; Behavior, Animal; Biomarkers - metabolism; Biting; brain; Brain damage; Brain Injuries - pathology; Brain injury; Brain stem; Brain Stem - pathology; Bromine; Bromine - administration & dosage; Bromine - adverse effects; Cages; Catecholamine; Catecholamines; Catecholamines - metabolism; Dopamine; Evaluation; Exposure; Fatty acids; Female; Glial fibrillary acidic protein; Glial Fibrillary Acidic Protein - metabolism; halogens; Heart; Hyperactivity; Industrial applications; injury; Lipid peroxidation; Metabolism; Metabolites; Metabolome; neuronal; Neurons - drug effects; Neurons - pathology; Neurotransmitter Agents - metabolism; Neurotransmitters; Oxidative stress; Oxidative Stress - drug effects; Proteins; Rats; Rats, Sprague-Dawley; Rodents; Sympathetic nervous system; Traumatic brain injury; Tryptophan; Tryptophan hydroxylase; Tryptophan Hydroxylase - metabolism; Tyrosine; Tyrosine 3-monooxygenase; Tyrosine 3-Monooxygenase - metabolism
• ISSN: 1422-0067; 1661-6596; 1422-0067
• DOI: 10.3390/ijms22126316

The risk of accidental bromine (Br ) exposure to the public has increased due to its enhanced industrial use. Inhaled Br damages the lungs and the heart; however, adverse effects on the brain are unknown. In this study, we examined the neurological effects of inhaled Br in Sprague Dawley rats. Rats were exposed to Br (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 Br 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 Br exposure.