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العنوان
A Study on the Toxicity of Cotton Pesticides on Freshwater Ecosystems =
المؤلف
Shaaban, Mona Shaaban Abdou.
هيئة الاعداد
مشرف / على عبد الهدى سعيد
مشرف / هشم زكى ابرهيم
مشرف / احمد السيد محمود
مشرف / هشم زكى
الموضوع
Toxicity of cotton.
تاريخ النشر
2012.
عدد الصفحات
81 p. :
اللغة
الإنجليزية
الدرجة
ماجستير
التخصص
علوم البيئة
تاريخ الإجازة
1/1/2012
مكان الإجازة
جامعة الاسكندريه - معهد الدراسات العليا والبحوث - Environmental studies
الفهرس
Only 14 pages are availabe for public view

from 99

from 99

Abstract

Insecticides are still of the most powerful weapons in our never ending battle against insect pests. Organophosphate (OP) and pyrethroid insecticides are two groups of insecticides still used up tell now for controlling the most insect pests. Among these insect pests is cotton leaf-worm, Spodopatera littoralis (Boisd.). The cotton leafworm, S. littoralis, is one of the most important economic pests and is a polyphagous insect pest which attacks many economic agricultural crops including cotton in Egypt (Farrag and Noussier, 1996)(1).
Toxicity of insecticides against the non-target insects is important as well as toxicity of insecticides against the target insects. Chironomus riparius as a non-target insect is widely used in toxicity tests. They are easy to culture, sensitive to many pollutants, and have a short life cycle (Ingersoll and Nelson, 1990)(2).Their ability to burrow into sediment also makes them good biological indicators for toxicants that may be adsorbed to sediments.
The extensive use of pesticides as well as their relatively high persistence in aquatic sediments may result in high concentrations of pesticides, especially in intensive agricultural areas (Mally, 1996)(3).
The organophosphorus insecticides are neurotoxic, although this group acts on the nervous system by inhibiting the enzyme acetyl cholinesterase (AChE) protein results in the formation of a transient, intermediate complex that partially hydrolyzes, leaving a stable, phosphorylated, and largely unreactive, inhibited enzyme that, under normal circumstances, can be reactivated only at very slow rate (Ecobichon, 1991 )(4). With many organophosphorus insecticides, an irreversible inhibited enzyme is formed, and the signs and symptoms of intoxication are prolonged and persistent. However, some organophosphorus insecticides are thought to be toxic only after metabolism by cytochrome P-450 monooxygenase enzyme systems. This bioactivation step creates a metabolite that is a much stronger inhibitor of the AChE than the parent compound (Belden and Lydy, 2000)(3).
Synthetic pyrethroids belong to the most used classes of insecticides. The pyrethroids show two different characteristic acidic portions, chrysanthemic or pyrethric acids resulting in type I and type II syndrome. Type II syndrome involves primarily an action in the central nervous system, whereas with the type I syndrome,--peripheral nerves are also involved (Ecobichon, 1991)(4). Both type I and II pyrethroid insecticides affect the sodium channels in the nerve membranes, causing repetitive neuronal discharge. There appears to be a prolongation of sodium influx with a delay in the closing of the sodium activation gate, resulting in prolonged sodium tail current (Narahashi, 1986; Bradbury and Coats, 1989; Ecobichon, 1991)(6, ,4). Type II pyrethroids prolongs the sodium channel open-time much more drastically than type I pyrethroids (Narahashi, 1986)(6). Also other sites of action have been noted for the pyrethroid insecticides.