Thirdhand Smoke Exposure Affects Mice Pancreas Microstructure

Eva Rianti Indrasari, Annisa Rahmah Furqaani, Listya Hanum Siswanti, Ihsan Muhammad Nauval, Putra Zam Zam Rachmatullah

Abstract


Cigarette residue toxins can accumulate in the body, including the pancreas, which potentially reduces pancreas function. In addition, the active compounds in cigarettes are reporting to interfere with an elevation of reactive oxygen species, leading to disruption of pancreatic microstructures. Furthermore, pancreatic cell dysfunction is responsible for developing diabetes mellitus disease. The objective of this study was to analyze the effect of thirdhand smoke exposure on mice pancreatic microstructure image. It was an in vivo laboratory experimental study with a completely randomized design at the Medical Biology Laboratory of the Universitas Islam Bandung from November 2020–June 2021. The subjects were 20 adult male mice aged 8–10 weeks, weighing 25–30 grams, in good health condition, and randomly divided into two groups (control group and treatment group exposed to thirdhand cigarette smoke for four weeks). After the completion of the exposure period, pancreatic cells isolation was performing. The parameters observed in this study were the number and diameter islet of Langerhans. Data analysis used the independent t test parametric (α=5%). The results showed that the number and diameter islet of Langerhans in the treated group were significantly lower than the control group (p<0.05). The average number in the control group was 9.40±3.20, while in the treatment group was 4.90±2.74 (28% smaller). The average diameter of control was 225.96±50.15 mm, while treatment was 162±49.68 mm (50% lower). In conclusion, thirdhand smoke exposure alters the pancreas microstructure. The toxic compounds on thirdhand cigarette smoke are involving in generating an elevation of free radical levels, depletion of antioxidants, and alteration of signal transduction resulted in acceleration of apoptosis rate of the islet of Langerhans, especially pancreatic β-cells.

 

PENGARUH PAPARAN ASAP ROKOK TERSIER PADA GAMBARAN MIKROSTRUKTUR PANKREAS MENCIT

Toksik residu rokok dapat terakumulasi pada tubuh, termasuk pankeas sehingga dapat menurunkan fungsi pankreas. Selain itu, senyawa aktif dalam rokok dilaporkan meningkatkan radikal bebas yang menyebabkan kerusakan mikrostruktur pankreas. Selanjutnya, disfungsi sel pankreas meningkatkan risiko diabetes melitus. Penelitian ini bertujuan menganalisis pengaruh asap rokok tersier terhadap gambaran mikrostruktur pankreas mencit. Penelitian ini merupakan penelitian eksperimental laboratorium in vivo dengan rancangan acak lengkap di Laboratorium Biologi Medik Universitas Islam Bandung periode November 2020–Juni 2021. Subjek penelitian adalah 20 mencit jantan dewasa berumur 8–10 minggu, bobot 25–30 gram, kondisi sehat, dan dibagi secara acak menjadi dua kelompok (kelompok kontrol dan kelompok perlakuan yang mendapat paparan asap rokok tersier selama empat minggu). Setelah periode pemberian paparan selesai, dilakukan isolasi sel pankreas. Parameter yang diamati dalam penelitian ini adalah jumlah dan diameter pulau Langerhans (islet of Langerhans). Analisis data menggunakan parametrik independent t test (α=5%). Hasil penelitian menunjukkan bahwa jumlah dan diameter pulau Langerhans pada kelompok perlakuan lebih rendah dibanding dengan kelompok kontrol (p<0,05). Jumlah rerata pada kelompok kontrol adalah 9,40±3,20, sedangkan pada kelompok perlakuan 4,90±2,74 (lebih rendah 28%). Diameter rerata pada kelompok kontrol adalah 225,96±50,19 mm dan kelompok perlakuan 162,89±49.68 mm (lebih rendah 50%). Simpulan, paparan asap rokok tersier dapat memengaruhi gambaran mikrostruktur pankreas. Senyawa toksik pada asap rokok tersier diduga terlibat dalam peningkatan kadar radikal bebas, penurunan kadar antioksidan, dan perubahan transduksi sinyal yang mengakibatkan peningkatan laju apoptosis pulau Langerhans, terutama sel β pankreas.


Keywords


Asap rokok tersier; β-cell pancreas; microstructure of pancreas; mikrostruktur pankreas; thirdhand smoke

Full Text:

PDF

References


Figueiró LR, Ziulkoski AL, Dantas DCM. Thirdhand smoke: when the danger is more than you can see or smell. Cad Saúde Pública. 2016;32(11):e00032216.

Bahl V, Shima HJ, Jacob P III, Dias K, Schick SF, Talbota P. Thirdhand smoke: chemical dynamics, cytotoxicity, and genotoxicity in outdoor and indoor environments. Toxicol In Vitro. 2016;32:220–31.

Sleiman M, Gundel LA, Pankow JF, Jacob P III, Singera BC, Destaillats H. Formation of carcinogens indoors by surface-mediated reactions of nicotine with nitrous acid, leading to potential thirdhand smoke hazards. Proc Natl Acad Sci USA. 2010;107(15):6576–81.

Hang B, Sarker AH, Havel C, Saha S, Hazra TK, Schick S, et al. Thirdhand smoke causes DNA damage in human cells. Mutagenesis. 2013;28(4):381–91.

Benowitz NL, Burbank AD. Cardiovascular toxicity of nicotine: implications for electronic cigarette use. Trends Cardiovasc Med. 2016;26(6):515–23.

Morris PB, Ference BA, Jahangir E, Feldman DN, Ryan JJ, Bahrami H, et al. Cardiovascular effects of exposure to cigarette smoke and electronic cigarettes: clinical perspectives from the Prevention of Cardiovascular Disease Section Leadership Council and Early Career Councils of the American College of Cardiology. J Am Coll Cardiol. 2015;66(12):1378–91.

Vallaster MP, Kukreja S, Bing XY, Ngolab J, Zhao-Shea R, Gardner PD, et al. Paternal nicotine exposure alters hepatic xenobiotic metabolism in offspring. eLife. 2017;6:e24771.

Esakky P, Hansen DA, Drury AM, Felder P, Cusumano A, Moley KH. Paternal exposure to cigarette smoke condensate leads to reproductive sequelae and developmental abnormalities in the offspring of mice. Reprod Toxicol. 2016;65:283‒94.

Alexandre M, Pandol SJ, Gorelick FS, Thrower EC. The emerging role of smoking in the development of pancreatitis. Pancreatology, 2011;11(5):469–74.

Topsakal S, Ozmen O, Aslankoc R, Aydemird DH. Pancreatic damage induced by cigarette smoke: the specific pathological effects of cigarette smoke in the rat model. Toxicol Res (Camb.). 2016;5(3):938–45.

Russell FA, King R, Smillie SJ, Kodji X, Brain SD. Calcitonin gene-related peptide: physiology and pathophysiology. Physiol Rev. 2014;94(4):1099–142.

Adhami N, Starck SR, Flores C, Martins Green M. A health threat to bystanders living in the homes of smokers: how smoke toxins deposited on surfaces can cause insulin resistance. PLoS One. 2016;11(3):e0208056.

Milnerowicz H, Śliwińska-Mossoń M, Sobiech KA. The effect of ozone on the expression of metallothionein in tissues of rats chronically exposed to cadmium. Environ Toxicol Pharmacol. 2017;52:27–37.

Chang KC, Hsu CC, Liu SH, Su CC, Yen CC, Lee MJ, et al. Cadmium induces apoptosis in pancreatic β-cells through a mitochondria-dependent pathway: the role of oxidative stress-mediated c-Jun N-terminal kinase activation. PLoS One. 2013;8(2):e54374.

Hermann PC, Sancho P, Cañamero M, Martinelli P, Madriles F, Michl P, et al. Nicotine promotes initiation and progression of KRAS-induced pancreatic cancer via Gata6-dependent dedifferentiation of acinar cells in mice. Gastroenterology. 2014;147(5):1119–33.e4.

Ario MD. Pengaruh nikotin dalam rokok pada diabetes melitus tipe 2. Majority. 2014;3(7):75–80.

Tong X, Chaudry Z, Lee C, Bone RN, Kanojia S, Maddatu J, et al. Cigarette smoke exposure impairs β-cell function through activation of oxidative stress and ceramide accumulation. Mol Metab. 2020;37:100975.

Nauval IM, Furqaani AR, Indrasari ER. Pengaruh paparan asap rokok tersier terhadap kadar glukosa darah mencit. JIKS. 2020;2(1):39–42.

Dai JB, Wang ZX, Qiao ZD. The hazardous effects of tobacco smoking on male fertility. Asian J Androl. 2015;17(6):954–60.

Fitzgerald R, Olsen A, Nguyen J, Wong W, El Muayed M, Edwards J. Pancreatic islets accumulate cadmium in a rodent model of cadmium-induced hyperglycemia. Int J Mol Sci. 2020;22(1):360.

Pietrobon CB, Lisboa PC, Bertasso IM, Peixoto TC, Soares PN, de Oliveira E, et al. Pancreatic steatosis in adult rats induced by nicotine exposure during breastfeeding. Endocrine. 2021;72(1):104–15.

Sun Q, Xu H, Xue J, Yang Q, Chen C, Yang P, et al. MALAT1 via microRNA-17 regulation of insulin transcription is involved in the dysfunction of pancreatic β-cells induced by cigarette smoke extract. J Cell Physiol. 2018;233(11):8862–73.

Oba S, Suzuki E, Yamamoto M, Horikawa Y, Nagata C, Takeda C, Gifu Diabetes Study Group. Active and passive exposure to tobacco smoke in relation to insulin sensitivity and pancreatic β-cell function in Japanese subjects. Diabetes Metab. 2015;41(2):160–7.

Zanini S, Renzi S, Limongi AR, Bellavite P, Giovinazzo F, Bermano G. A review of lifestyle and environment risk factors for pancreatic cancer. Eur J Cancer. 2021;145:53–70.

Menini S, Iacobini C, de Latouliere L, Manni I, Ionta V, Blasetti Fantauzzi C, et al. The advanced glycation end-product Nε-carboxymethyllysine promotes progression of pancreatic cancer: implications for diabetes-associated risk and its prevention. J Pathol. 2018;245(2):197–208.




DOI: https://doi.org/10.29313/gmhc.v9i2.8039

pISSN 2301-9123 | eISSN 2460-5441


Visitor since 19 October 2016: 

View My Stats


Free counters!


This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International License.