INTERACTION STUDIES BETWEEN LINDANE (GAM MA LIN -20®) AND DIMETHOATE (ROGOR®) IN VIVO AND IN VITRO

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Date
1998-09
Authors
GADAKA , MADU ADAMU
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Abstract
The toxicity of lindane and dimethoale has been studied individually and in combination in laboratory animals both in vivo and in vitro. Effects of lindane pretreatmenl on the toxicity of dimethoate was examined in acute and sub-chronic toxicity studies. The median lethal dose (LD50) for lindane and dimethoate were determined in wister strain rats by intraperitoneal route as 29.5 mg/kg and 185 mg/kg respectively. Symptoms of poisoning for lindane (hyper-excitation, tremor, conclusions) and dimethoate (swaying gait, respiratory distress, convulsion) were dose-dependent in severity. Lindane (1mg/kg, i.p) daily administration for seven days increaesd dimethoate LD50 in rats by 29.5%. The survival time in mice exposed to lethal dose of dimethoate (400 mg/kg) was also increased by 27.5% compared to control. Antidotal therapy trial against acute lindane poison was also carried out in mice using diazepam, phenobarbitone and phenytoin. All three agents produced dose-dependent alleviation of symptoms and as well increased survival rates. The highest trial dose of phenytoin (40 mg/kg). phenobaritone (20 mg/kg) and diazepam (10 mg/kg) resulted in 50%, 62.5% and 75% survival rales respectively. The control group produced 12.5% survival rate. EEG studies in rats showed desynchronization of the reticular formation (RF;) wave pattern due to lindane which effect was potentialed by dimethoale. Lindane-induced desynchronization was reversed by diazepam and phenytoin. Twelve weeks sub-chronic toxicity studies in rats investigated the effect of combined exposure to weekly lindane (10 mg/kg, i.p) and daily dimethoate (10, 25, 50. 75 mg/kg feed) oral administration. Control group receive normal Iced and no lindane treatment. At intervals of four weeks, rats were killed blood samples collected for enzyme assay, serum albumin and total bilirubin were determined. Liver, kidney and intestines were removed for histopathologic examinations. Serum transaminase (AST and ALT) activities showed general elevation in the dimethoatefed compared to control animals. Furthermore, AST and ALT activities were slightly higher in lindane-frce compared to lindane-treated dimethoate sub-groups throughout the twelve weeks exposure period. Serum AST activities were significantly (P < 0.05 - P - 0.01) higher in the dimethoate-fed animals in the presence and absence of lindane at four and eight weeks exposure, while activities were insignificantly laised at twelve weeks. Serum ALT activities on the other hand were significantly elevated (P < 0.02 - P < 0.001) at eight and twelve weeks while activities showed insignificant eleva'ion at four weeks exposure compared to control values. Activities of serum ALT were significantly raised (P < 0.05 - P < 0.001) at four weeks but dropped significantly (P < 0.05 - P - 0.01) below control activity at eight weeks. Activity returned to control levels at twelve weeks exposure. Serum albumin levels showed an insignificant decrease over control value at four weeks. However, significantly lower levels (P < 0.05 - P < 0.001) were observed at eight and twelve weeks exposure. No clear pattern was however, observed between lindane-free and vii lindane-treated groups in the serum.albumin levels. Levels for total bilirubin showed a gradual increase with duration of exposure, being insignificantly different from control at four weeks and significantly (P < 0.02 - P < 0.001) elevated at twelve weeks. Values for total bilirubin were higher in the presence of lindane treatment. Histopathologic examination after twelve weeks exposure period revealed no lesions in the kidneys and the intestines at all dose levels. However, the liver revealed various degree of fatty degeneration, the ocurrence of which showed correlation in extent of damage to period of exposure, rather than dimethoate dose or lindane treatment. Experiments using isolated rabbits ileum and rat phrenic nerve-diaphragm preparations showed a biphasie response by lindane, with stimulation at low doses and inhibition at high dose. Dimethoate dose-dependently potentiated cholinergic responses at both nicotinic and muscarinic receptors. Dimethoate (8 ng/ml) response was augmented by physosligmine (2.6 ng/ml) and antagonized by atropine (2 ng/ml), while d-tubocurarine (1.3 ng/ml) attenuated both dimethoate (60 ng/ml) and lindane (4.3 ng/ml) response at the neuromuscular junction. Lindane (6.4 ng/ml) attenuated dimethoate (8 ng/ml-) response and attenuated both spontaneous rabbit ileum and nerve twitch responses. The effect of lindane was augmented by d-tubocurarine (1.3 ng/ml) and attenuated by lignocaine (16.8 ng/ml). Lignocaine similarly attenuated dimethoate (60 ng/ml) response on the nerve. The findings of these studies suggest some degree of protection provided by lindane against dimethoate toxicity. The protective effect of lindane was pronounced in acute dimethoate administration and less so in sub-chronic concurrent exposure. The in vitro results indicate antagonism of dimethoate response by lindane. Combined pesticides exposure, therefore, need not necessarily imply exaggerated toxicity.
Description
A thesis in the department of PharmacoIogy and Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Ahmadu Bello University', Zaria, submitted to the Postgraduate School in partial fulfillment of the requirement for the award of degree of Doctor of Philosophy. Ahmadu Bello University, Zaria. SEPTEMBER. 1998.
Keywords
INTERACTION,, STUDIES,, LINDANE,, (GAM MA LIN -20®), DIMETHOATE, (ROGOR®), VIVO,, VITRO.
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