{'fraction_non_alphanumeric': 0.021632251720747297, 'fraction_numerical': 0.003933136676499509, 'mean_word_length': 5.2073170731707314, 'pattern_counts': {'":': 0, '<': 0, '<?xml version=': 0, '>': 0, 'https://': 0, 'lorem ipsum': 0, 'www.': 0, 'xml': 0}, 'pii_count': 0, 'substrings_counts': 0, 'word_list_counts': {'cursed_substrings.json': 0, 'profanity_word_list.json': 0, 'sexual_word_list.json': 0, 'zh_pornsignals.json': 0}}
Neurotoxic action of chlorinated hydrocarbon insecticides.

Evidence on the mode of action of chlorinated hydrocarbon insecticides is reviewed and discussed. DDT and its analogs act mainly at the nerve axon by interfering with Na+ and K+ conductance gating. Various analogs show excitatory, blocking or both kinds of action depending on whether they interfere with Na-inactivation, activation or both. These actions may be functionally related to inhibition of an ecto Ca2+ ATPase, but at this time there is insufficient evidence to draw that conclusion. Bicyclodienes, lindane and mirex and certain of its analogs act at presynaptic terminals to enhance the release of neurotransmitter. Direct evidence to this action by some compounds is available on cholinergic and glutaminergic junctions, but other kinds of junctions may be affected. This action may be functionally related to inhibition of Ca2+-Mg2+ ATPase which is thought to be identical with the Ca2+ ion pump that maintains low internal Ca+ concentrations.