G J Singh, B Singh
Index: Neurobehav. Toxicol. Teratol. 6(3) , 201-13, (1984)
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Cellular lesions in the metathoracic ganglion of P. americana following insecticide treatment have been examined. Treatment of the isolated ganglia with dieldrin (10 microM) and bioresmethrin (5 microM) induced mitochondrial damage in the neuropile and nerve cell bodies. The mitochondria in treated nerve cells were swollen with broken cristae and devoid of normal morphological appearance. Following in vivo treatment of cockroaches with these insecticides, this type of mitochondrial damage was observed even at the onset of poisoning. In the prostrate cockroaches, however, the mitochondrial swelling was accompanied by the accumulation of electron dense granules. In addition, the neuropiles of insecticide-treated ganglia contained secondary lysosomes which increased in size and number with the progress of poisoning and showed signs of depletion of synaptic vesicles. The action of dieldrin upon the ultrastructure was completely abolished by pretreatment of ganglia with 10 mM Mg2+. On the other hand, pretreatment of ganglia with tetrodotoxin and pentobarbital-sodium had very little effect on the action of dieldrin though these compounds blocked the action of bioresmethrin. The results of this study suggest that cellular lesions in the insect CNS, caused by dieldrin, are due to an enhanced uptake of calcium into nerve terminals which may occur independent of membrane depolarization. The effects of bioresmethrin upon the ultrastructure of the CNS are apparently mediated by nerve excitation and membrane depolarization. It is concluded that treatment of intact cockroaches with dieldrin and bioresmethrin initiates catabolic processes in the nerve cells leading to cellular lesions which are indicative of neuronal degeneration.
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