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Behavioral and Neuronal Effects of Inhaled Bromine Gas: Oxidative Brain Stem Damage
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...
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| Published in: | International journal of molecular sciences 2021-06, Vol.22 (12), p.6316 |
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| container_title | International journal of molecular sciences |
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| creator | 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 |
| description | 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. |
| doi_str_mv | 10.3390/ijms22126316 |
| format | article |
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) 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.</description><identifier>ISSN: 1422-0067</identifier><identifier>ISSN: 1661-6596</identifier><identifier>EISSN: 1422-0067</identifier><identifier>DOI: 10.3390/ijms22126316</identifier><identifier>PMID: 34204780</identifier><language>eng</language><publisher>Switzerland: MDPI AG</publisher><subject>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</subject><ispartof>International journal of molecular sciences, 2021-06, Vol.22 (12), p.6316</ispartof><rights>2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2021 by the authors. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c478t-c94ee7ef138d0cbbc20d013ac3b0968cae025b7adcb5c6df5d1f7edcbd8c6c083</citedby><cites>FETCH-LOGICAL-c478t-c94ee7ef138d0cbbc20d013ac3b0968cae025b7adcb5c6df5d1f7edcbd8c6c083</cites><orcidid>0000-0003-1049-5054</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2544995253/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2544995253?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25753,27924,27925,37012,44590,53791,53793,75126</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34204780$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shakil, Shazia</creatorcontrib><creatorcontrib>Masjoan Juncos, Juan Xavier</creatorcontrib><creatorcontrib>Mariappan, Nithya</creatorcontrib><creatorcontrib>Zafar, Iram</creatorcontrib><creatorcontrib>Amudhan, Apoorva</creatorcontrib><creatorcontrib>Amudhan, Archita</creatorcontrib><creatorcontrib>Aishah, Duha</creatorcontrib><creatorcontrib>Siddiqui, Simmone</creatorcontrib><creatorcontrib>Manzoor, Shajer</creatorcontrib><creatorcontrib>Santana, Cristina M</creatorcontrib><creatorcontrib>Rumbeiha, Wilson K</creatorcontrib><creatorcontrib>Salim, Samina</creatorcontrib><creatorcontrib>Ahmad, Aftab</creatorcontrib><creatorcontrib>Ahmad, Shama</creatorcontrib><title>Behavioral and Neuronal Effects of Inhaled Bromine Gas: Oxidative Brain Stem Damage</title><title>International journal of molecular sciences</title><addtitle>Int J Mol Sci</addtitle><description>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.</description><subject>4-Hydroxynonenal</subject><subject>Administration, Inhalation</subject><subject>Aggressiveness</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Autonomic nervous system</subject><subject>Behavior</subject><subject>Behavior, Animal</subject><subject>Biomarkers - metabolism</subject><subject>Biting</subject><subject>brain</subject><subject>Brain damage</subject><subject>Brain Injuries - pathology</subject><subject>Brain injury</subject><subject>Brain stem</subject><subject>Brain Stem - pathology</subject><subject>Bromine</subject><subject>Bromine - administration & dosage</subject><subject>Bromine - adverse effects</subject><subject>Cages</subject><subject>Catecholamine</subject><subject>Catecholamines</subject><subject>Catecholamines - metabolism</subject><subject>Dopamine</subject><subject>Evaluation</subject><subject>Exposure</subject><subject>Fatty acids</subject><subject>Female</subject><subject>Glial fibrillary acidic protein</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>halogens</subject><subject>Heart</subject><subject>Hyperactivity</subject><subject>Industrial applications</subject><subject>injury</subject><subject>Lipid peroxidation</subject><subject>Metabolism</subject><subject>Metabolites</subject><subject>Metabolome</subject><subject>neuronal</subject><subject>Neurons - drug effects</subject><subject>Neurons - pathology</subject><subject>Neurotransmitter Agents - metabolism</subject><subject>Neurotransmitters</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Sympathetic nervous system</subject><subject>Traumatic brain injury</subject><subject>Tryptophan</subject><subject>Tryptophan hydroxylase</subject><subject>Tryptophan Hydroxylase - metabolism</subject><subject>Tyrosine</subject><subject>Tyrosine 3-monooxygenase</subject><subject>Tyrosine 3-Monooxygenase - 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) 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.</abstract><cop>Switzerland</cop><pub>MDPI AG</pub><pmid>34204780</pmid><doi>10.3390/ijms22126316</doi><orcidid>https://orcid.org/0000-0003-1049-5054</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1422-0067 |
| ispartof | International journal of molecular sciences, 2021-06, Vol.22 (12), p.6316 |
| issn | 1422-0067 1661-6596 1422-0067 |
| language | eng |
| recordid | cdi_doaj_primary_oai_doaj_org_article_34ca3c87d89d4a29bd9170ded20315e4 |
| source | Publicly Available Content Database; PubMed Central |
| 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 |
| title | Behavioral and Neuronal Effects of Inhaled Bromine Gas: Oxidative Brain Stem Damage |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T06%3A26%3A55IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_doaj_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Behavioral%20and%20Neuronal%20Effects%20of%20Inhaled%20Bromine%20Gas:%20Oxidative%20Brain%20Stem%20Damage&rft.jtitle=International%20journal%20of%20molecular%20sciences&rft.au=Shakil,%20Shazia&rft.date=2021-06-12&rft.volume=22&rft.issue=12&rft.spage=6316&rft.pages=6316-&rft.issn=1422-0067&rft.eissn=1422-0067&rft_id=info:doi/10.3390/ijms22126316&rft_dat=%3Cproquest_doaj_%3E2544995253%3C/proquest_doaj_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c478t-c94ee7ef138d0cbbc20d013ac3b0968cae025b7adcb5c6df5d1f7edcbd8c6c083%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2544995253&rft_id=info:pmid/34204780&rfr_iscdi=true |