کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
5859561 | 1132482 | 2012 | 8 صفحه PDF | دانلود رایگان |
عنوان انگلیسی مقاله ISI
Biochemical, histopathological and clinical evaluation of delayed effects caused by methamidophos isoforms and TOCP in hens: Ameliorative effects using control of calcium homeostasis
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کلمات کلیدی
OPIDNToCPTri-ortho-cresyl phosphateNTELD50OECDIC50AChE - آهیAcetylcholinesterase - استیل کولین استرازstandard deviation - انحراف معیارOrganisation for Economic Co-operation and Development - سازمان همکاری اقتصادی و توسعهOrganophosphorus pesticide - سموم دفع آفات فسفرMethamidophos - متامیدوفوسmedian lethal dose - میانگین دوز مرگبارneuropathy target esterase - نوراستیک هدف استرازOrganophosphorus-induced delayed neuropathy - نوروپاتی تاخیر ناشی از اتانول فسفرCalpain - کالپینCalcium gluconate - گلوکونات کلسیم
موضوعات مرتبط
علوم زیستی و بیوفناوری
علوم محیط زیست
بهداشت، سم شناسی و جهش زایی
پیش نمایش صفحه اول مقاله
![عکس صفحه اول مقاله: Biochemical, histopathological and clinical evaluation of delayed effects caused by methamidophos isoforms and TOCP in hens: Ameliorative effects using control of calcium homeostasis Biochemical, histopathological and clinical evaluation of delayed effects caused by methamidophos isoforms and TOCP in hens: Ameliorative effects using control of calcium homeostasis](/preview/png/5859561.png)
چکیده انگلیسی
This work evaluated the potential of the isoforms of methamidophos to cause organophosphorus-induced delayed neuropathy (OPIDN) in hens. In addition to inhibition of neuropathy target esterase (NTE) and acetylcholinesterase (AChE), calpain activation, spinal cord lesions and clinical signs were assessed. The isoforms (+)-, (±)- and (â)-methamidophos were administered at 50 mg/kg orally; tri-ortho-cresyl phosphate (TOCP) was administered (500 mg/kg, po) as positive control for delayed neuropathy. The TOCP hens showed greater than 80% and approximately 20% inhibition of NTE and AChE in hen brain, respectively. Among the isoforms of methamidophos, only the (+)-methamidophos was capable of inhibiting NTE activity (approximately 60%) with statistically significant difference compared to the control group. Calpain activity in brain increased by 40% in TOCP hens compared to the control group when measured 24 h after dosing and remained high (18% over control) 21 days after dosing. Hens that received (+)-methamidophos had calpain activity 12% greater than controls. The histopathological findings and clinical signs corroborated the biochemical results that indicated the potential of the (+)-methamidophos to be the isoform responsible for OPIDN induction. Protection against OPIDN was examined using a treatment of 2 doses of nimodipine (1 mg/kg, i.m.) and one dose of calcium gluconate (5 mg/kg, i.v.). The treatment decreased the effect of OPIDN-inducing TOCP and (+)-methamidophos on calpain activity, spinal cord lesions and clinical signs.
ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Toxicology - Volume 302, Issue 1, 8 December 2012, Pages 88-95
Journal: Toxicology - Volume 302, Issue 1, 8 December 2012, Pages 88-95
نویسندگان
Guilherme L. Emerick, Marion Ehrich, Bernard S. Jortner, Regina V. Oliveira, Georgino H. DeOliveira,