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Nikbakht, M., Ashrafi-Kooshk, M., jaafari, M., Ghasemi, M., Khodarahmi, R. (2014). Does Long-Term Administration of a Beta-Blocker (Timolol) Induce Fibril-Based Cataract Formation In-vivo?. Iranian Journal of Pharmaceutical Research, 13(2), 599-611. doi: 10.22037/ijpr.2014.1520
Mohammad Reza Nikbakht; Mohammad Reza Ashrafi-Kooshk; morteza jaafari; Moosa Ghasemi; Reza Khodarahmi. "Does Long-Term Administration of a Beta-Blocker (Timolol) Induce Fibril-Based Cataract Formation In-vivo?". Iranian Journal of Pharmaceutical Research, 13, 2, 2014, 599-611. doi: 10.22037/ijpr.2014.1520
Nikbakht, M., Ashrafi-Kooshk, M., jaafari, M., Ghasemi, M., Khodarahmi, R. (2014). 'Does Long-Term Administration of a Beta-Blocker (Timolol) Induce Fibril-Based Cataract Formation In-vivo?', Iranian Journal of Pharmaceutical Research, 13(2), pp. 599-611. doi: 10.22037/ijpr.2014.1520
Nikbakht, M., Ashrafi-Kooshk, M., jaafari, M., Ghasemi, M., Khodarahmi, R. Does Long-Term Administration of a Beta-Blocker (Timolol) Induce Fibril-Based Cataract Formation In-vivo?. Iranian Journal of Pharmaceutical Research, 2014; 13(2): 599-611. doi: 10.22037/ijpr.2014.1520

Does Long-Term Administration of a Beta-Blocker (Timolol) Induce Fibril-Based Cataract Formation In-vivo?

Article 27, Volume 13, Issue 2, Spring 2014, Page 599-611  XML PDF (1.72 MB)
Document Type: Research article
DOI: 10.22037/ijpr.2014.1520
Authors
Mohammad Reza Nikbakht1; Mohammad Reza Ashrafi-Kooshk2; morteza jaafari3; Moosa Ghasemi1; Reza Khodarahmi email 4
1Faculty of Pharmacy, Kermanshah University of Medical Sciences, Kermanshah, Iran
2Medical Biology Research Center, Kermanshah University of Medical Sciences, Kermanshah, Iran
3MBRC
4Medical Biology Research Center, Kermanshah University of Medical Science, Kermanshah, Iran
Abstract
Timolol is a non-selective beta-adrenergic receptor antagonist administered for treating glaucoma, heart attacks and hypertension. In the present study, we set out to determine whether or not timolol can provoke cataract formation, thus the influence of timolol on the amyloid-type aggregation of crystallin was investigated. We then provided experimental evidence of crystallin aggregation and its induction by timolol using different spectroscopic measurements. Turbidimetric measurements as well as ThT fluorescence data indicated that timolol induce extent of crystallin amyloid formation. The kinetic of protein aggregation was also changed in presence of increasing concentrations of the drug suggesting that long-term drug administration may contribute to the development of cataract. Since the consequence of timolol-crystallin interaction has yet to be identified, additional data on it may help us to postpone amyloid cataract formation.
Keywords
Timolol; Amyloid; Cataract; Crystallin
Main Subjects
toxicology and Pharmacology
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