Dynamics in the content of the cytokines in the bronchoalveolar lavage fluid in rats after acute inhalation intoxication by clorine and pyrolysis products, containing hydrogen chloride

Abstract

It is known that inhalation exposure to chlorine and hydrogen chloride leads to damage to the respiratory system up to the development of acute pulmonary edema in victims. No data on the mechanisms of development of pulmonary edema upon exposure to hydrogen chloride have been found in the available literature. The study was carried out on white outbred male rats, which were divided into 3 groups: Group I — control; Group II — animals were intoxicated with chlorine at a dose of 1.5 median lethal concentration (30 min); Group III — animals were intoxicated with hydrogen chloride at a dose of 1.5 median lethal concentration (30 min). Immediately after exposure to the studied toxicants, as well as after 1, 3 and 6 h, the lung coefficient and the content of cytokines (interleukins-1β, 6, 10 and interferon-γ) in the bronchoalveolar lavage fluid were determined in animals. It was revealed that an increase in the lung coefficient (p < 0.05) in animals in groups II and III was accompanied by a significant increase (1.5 times) in the content of the studied cytokines in the bronchial-alveolar lavage fluid compared with animals in group I. III an increase (p < 0.05) in the content of cytokines is recorded later — only 3 hours after exposure, while it is significantly lower than in animals of group II at all studied periods. Thus, intoxication with hydrogen chloride leads to a slower development of pulmonary edema and an increase in the content of both pro (interleukins-1β, 6) and anti-inflammatory cytokines (interleukin-10, interferon-γ) in the bronchial-alveolar lavage fluid compared to animals, exposed to chlorine intoxication.

Keywords

intoxication / toxic pulmonary edema / cytokines / interleukin-1β / interleukin-6 / interleukin-10 / interferon-γ

References

[1] Torkunov PA, Shabanov PD. Pulmonary edema: pathogenesis, modeling, methodology for studying. Reviews on clinical pharmacology and drug therapy. 2009;6(2):3–54. (In Russ.)

[2] Торкунов П.А., Шабанов П.Д. Токсический отек легких: патогенез, моделирование, методология изучения // Обзоры по клинической фармакологии и лекарственной терапии. 2008. Т. 6, № 2. С. 42–54.

[3] White CW, Martin JG. Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models. Proceedings of the American Thoracic Society. 2010;7(4):257–263. doi: 10.1513/pats.201001-008SM

[4] White C.W., Martin J.G. Chlorine gas inhalation: human clinical evidence of toxicity and experience in animal models // Proceedings of the American Thoracic Society. 2010. Vol. 7, No. 4. P. 257–263. doi: 10.1513/pats.201001-008SM

[5] World Health Organization. International statistical classification of diseases and related health problems. World Health Organization. 2004;1(1):698. (In Russ.)

[6] Международная статистическая классификация болезней и проблем, связанных со здоровьем; 10-й пересмотр. Женева: ВОЗ. 2004. Т. 1, ч. 1. 698 с.

[7] Barrow CS, Alarie Y, Warrick JC, et al. Comparison of the sensory irritation response in mice to chlorine and hydrogen chloride. Archives of Environmental Health: An International Journal. 1977;32(2):68–76. Doi: 10.1080/00039896.1977.10667258

[8] Barrow C.S., Y. Alarie, J.C. Warrick, et al. Comparison of the sensory irritation response in mice to chlorine and hydrogen chloride // Archives of Environmental Health: An International Journal. 1977. Vol. 32, No. 2. P. 68–76. Doi: 10.1080/00039896.1977.10667258

[9] Miller SN. Acute toxicity of respiratory irritant exposures. The Toxicant Induction of Irritant Asthma, Rhinitis, and Related Conditions. Boston: Springer. 2013;83–101. Doi: 10.1007/978-1-4614-9044-9_4

[10] Miller S.N. Acute toxicity of respiratory irritant exposures. The Toxicant Induction of Irritant Asthma, Rhinitis, and Related Conditions. Boston: Springer; 2013. P. 83–101. Doi: 10.1007/978-1-4614-9044-9_4

[11] Potapov PK, Dimitriev YuV, Tolkach PG. Ctrukturno-funkcional’nye narusheniya dyhatel’noj sistemy u laboratornyh zhivotnyh pri intoksikacii produktami piroliza hlorsoderzhashchih polimernyh materialov. Medicinskij akademicheskij zhurnal. 2020;(3):13–22. (In Russ.)

[12] Потапов П.К., Димитриев Ю.В., Толкач П.Г. Cтруктурно-функциональные нарушения дыхательной системы у лабораторных животных при интоксикации продуктами пиролиза хлорсодержащих полимерных материалов // Медицинский академический журнал. 2020. № 3. C. 13–22.

[13] Banadykov KD, Lyutenko ER, Alibekova AI, et al. Sovremennye aspekty toksicheskogo dejstviya hlora. Tverskoj medicinskij zhurnal. 2016;(2):21–22. (In Russ.)

[14] Банадыков К.Д., Лютенко Э.Р., Алибекова А.И., и др. Современные аспекты токсического действия хлора // Тверской медицинский журнал. 2016. № 2. С. 21–22.

[15] Ketlinsky SA, Simbirtsev AS. Cytokines. St. Petersburg: Folio, 2008. (In Russ.)

[16] Кетлинский С.А., Симбирцев А.С. Цитокины. СПб.: Фолиант, 2008. 552 с

[17] Chuchalin AG. Biologicheskie markery pri respiratornyh zabolevaniyah. Terapevticheskij arhiv. 2014;86(3):4–13. (In Russ.)

[18] Чучалин А.Г. Биологические маркеры при респираторных заболеваниях // Терапевтический архив. 2014. Т. 86, № 3. С. 4–13.

[19] Directive 2010/63/EU of the European Parliament and of the Council of the European Union on the protection of animals used for scientific purposes, dated 22 September 2010. (In Russ.)

[20] Директива 2010/63/EU Европейского парламента и совета европейского союза по охране животных, используемых в научных целях НП объединение специалистов по работе с лабораторными животными. СПб.: Rus-LASA, 2012. 48 с.

[21] Beck G. Etude cyto-bactériologique quantitative de l’expectoration chez le bronchiteux chronique. Revue francaise des maladies respiratoires. 1980;8(5):357–366. (In Fr.)

[22] Beck G. Etude cyto-bactériologique quantitative de l’expectoration chez le bronchiteux chronique // Revue francaise des maladies respiratoires. 1980. Vol. 8, No. 5. P. 357–366.

[23] Davidjuk OV, Docenko AM, Kosolapov DA. Ponjatie i provedenie probit-analiza pri reshenii zadach kolichestvennoj ocenki riska avarij. Bezopasnost’ truda v promyshlennosti. 2009;4:48–51. (In Russ.)

[24] Давидюк О.В., Доценко А.М., Косолапов Д.А. Понятие и проведение пробит-анализа при решении задач количественной оценки риска аварий // Безопасность труда в промышленности. 2009. № 4. С. 48–51.

[25] Pugach VA, Tyunin MA, Vlasov TD, et al. Biomarkery ostrogo respiratornogo distress-sindroma: problemy i perspektivy ih primeneniya. Vestnik anesteziologii i reanimatologii. 2019;16(4):38–46. (In Russ.)

[26] Пугач В.А., Тюнин М.А., Власов Т.Д., и др. Биомаркеры острого респираторного дистресс-синдрома: проблемы и перспективы их применения // Вестник анестезиологии и реаниматологии. 2019. Т. 16, № 4. C. 38–46.

[27] Serebrennikova SN, Seminskij IZh. Rol’ citokinov v vospalitel’nom processe (soobshchenie 1). Sibirskij medicinskij zhurnal. 2008;81(6):5–8. (In Russ.)

[28] Серебренникова С.Н., Семинский И.Ж. Роль цитокинов в воспалительном процессе (сообщение 1) // Сибирский медицинский журнал. 2008. Т. 81, № 6. С. 5–8.

[29] Chuchalin AG. Pulmonary oedema: physiology of lung circulation, pathophysiology of pulmonary oedema. Russian pulmonology journal. 2005;(21):1374–1382. (In Russ.). doi: 10.18093/0869-0189-2005-0-4-9-18

[30] Чучалин А.Г. Отек легких: физиология легочного кровообращения и патофизиология отека легких // Русский медицинский журнал. 2005. № 21. С. 1374–1382. Doi: 10.18093/0869-0189-2005-0-4-9-18

[31] Rodionov GG, Hurcilava OG, Pluzhnikov NN, et al. Oksidativnyj stress i vospalenie: patogeneticheskoe partnerstvo. Saint Petersburg: Severo-Zapadnyj gosudarstvennyj medicinskij universitet im. I.I. Mechnikova, 2012. 340 p. (In Russ.)

[32] Родионов Г.Г., Хурцилава О.Г., Плужников Н.Н., и др. Оксидативный стресс и воспаление: патогенетическое партнерство. СПб.: Северо-Западный государственный медицинский университет им. И.И. Мечникова, 2012. 340 c.

RIGHTS & PERMISSIONS

Potapov P.K., Gennad`evich P.G., Rogovskaya N.Y., Babakov V.N., Basharin V.A.