Evaluation of the protective effects of atropine and diazepam against cypermethrin induced lethality
4
Issued Date
2024
Copyright Date
1990
Resource Type
Language
eng
File Type
application/pdf
No. of Pages/File Size
ix, 95 leaves : ill.
Access Rights
open access
Rights
ผลงานนี้เป็นลิขสิทธิ์ของมหาวิทยาลัยมหิดล ขอสงวนไว้สำหรับเพื่อการศึกษาเท่านั้น ต้องอ้างอิงแหล่งที่มา ห้ามดัดแปลงเนื้อหา และห้ามนำไปใช้เพื่อการค้า
Rights Holder(s)
Mahidol University
Bibliographic Citation
Thesis (M.Sc. (Toxicology))--Mahidol University, 1990
Suggested Citation
Punthip Teeyapant Evaluation of the protective effects of atropine and diazepam against cypermethrin induced lethality. Thesis (M.Sc. (Toxicology))--Mahidol University, 1990. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/99875
Title
Evaluation of the protective effects of atropine and diazepam against cypermethrin induced lethality
Alternative Title(s)
การประเมินประสิทธิภาพของไดอะซีแพนและอะโทรปีนในการป้องกันการตายของสัตว์เนื่องจากไซเพอร์เมทริน
Author(s)
Abstract
The protective effects of atropine and diazepam against cypermethrin induced lethality were evaluated in mice. Diazepam was used clinically to control convulsion induced by toxic dose of cypermethrin. It was found that diazepam delayed the onset of death induced by cypermethrin but not AZCORD R. Diazepam 5 mg/kg can reduce the mortality induced by both cypermethrin and AZCORD R only 15-20%, and increasing the dose of diazepam does not produce more reduction in lethality. Atropine can significantly delay the onset of death induced by cypermethrin but not by AZCORD (R) or monocrotophos. Low doses of atropine given 30 minutes before the administration of pesticides are very effective in reducing the percent lethality induced by cypermethrin, AZCORD (R) and monocrotophos. The protective effect of atropine suggested that the toxidc effects of cypermethrin are related to acetylcholine. Overactivity of muscarinic cholinergic function can be the consequence of increased acetylcholine relase and/or inhibition of the cholinesterase activity. In this study, cypermethrin didnot inhibit serum cholinesterase and red blood cell acetylcholinesterase. It is likely that the cholinergic muscarinic overactivity is the result of stimulation of ACh release as reported by the other group of investigators. The results of our study suggested that peripheral muscarinic overstimulation was the major cause of death of cypermethrin-induced lethality in mice. The addition of diazepam did not produce additive protective effect.
Description
Toxicology (Mahidol University 1990)
Degree Name
Master of Science
Degree Level
Master's degree
Degree Department
Faculty of Science
Degree Discipline
Toxicology
Degree Grantor(s)
Mahidol University