heptahydrate brands

Molecular formula: C10H5Cl7

EVIDENCE INDICATES THAT CYCLODIENE-TYPE-INSECTICIDES, EG, HEPTACHLOR EPOXIDE, MIMIC ACTION OF PICROTOXININ. THESE INSECTICIDES INHIBIT THE GAMMA-AMINOBUTYRIC ACID-STIMULATED CHLORIDE UPTAKE IN COXAL MUSCLE OF AMERICAN COCKROACH, & DIRECTLY COMPETE AGAINST LABELED DIHYDROPICROTOXININ FOR BINDING IN THE RAT BRAIN SYNAPTOSOMES. MOREOVER, SEVERAL CYCLODIENE RESISTANT INSECT STRAINS ARE RESISTANT TO PICROTOXININ. THIS CROSS-RESISTANCE IS SPECIFIC TO PICROTOXININ & DOES NOT EXTEND TO OTHER NEUROEXCITANTS. THESE INSECTICIDES, LIKE PICROTOXININ, CAUSE CENTRAL NERVOUS EXCITATION BY STIMULATING TRANSMITTER RELEASE. THESE RESULTS INDICATE THAT SOME OF THE NERVE EXCITATION SYMPTOMS THAT INSECTICIDES CAUSE ARE LIKELY DUE TO THEIR INTERACTION WITH PICROTOXININ RECEPTOR. HEPTACHLOR WAS EVALUATED FOR GENOTOXICITY & EPIGENETIC MEMBRANE EFFECTS. IT WAS NON-GENOTOXIC IN ARLHGPRT MUTAGENESIS ASSAY IN WHICH THE GENOTOXIC CARCINOGENS 7,12-DIMETHYLBENZ(A)ANTHRACENE & BENZO(A)PYRENE INDUCED SIGNIFICANT INCR IN MUTANT INCIDENCE. HEPTACHLOR INHIBITED INTERCELLULAR COMMUNICATION BETWEEN CULTURED LIVER CELLS, A PROPERTY DEMONSTRATED BY MANY TUMOR PROMOTING AGENTS, WHEREAS, BENZO(A)PYRENE DID NOT PRODUCE THIS EPIGENETIC EFFECT. The actions of the polychlorocycloalkane insecticide heptachlor, and its epoxide metabolite, were examined on GABA receptors in insects and vertebrates. Electrophysiological experiments on the cell body of the cockroach (Periplaneta americana) fast coxal depressor motor neuron (Df), and GABA-activated (36) Cl- uptake experiments on microsacs perpared from cockroach ventral nerve cords showed that both heptachlor and heptachlor epoxide blocked functional GABA receptors. The block appeared to be non-competitive and was voltage-independent over the membrane potential range -75 mV to -110 mV. There was no significant difference between the potencies of heptachlor and heptachlor epoxide in the functional assays for insect GABA receptors. Both compounds inhibited (35)S-t-butylbicyclophosphorothionate binding in insects and vertebrates. The findings provide further evidence for block of an insect GABA receptor/Cl- channel by the cyclodiene class of polychlorocycloalkanes, and reveal differences in the insecticide (35)S-t-butylbicyclophosphorothionate binding site interactions of insects and vertebrates. The effects of heptachlor on oxidative phosphorylation and electron transport in male Donryu rat liver mitochondria were investigated. The effects of 50 uM heptachlor on the respiratory activity of isolated liver mitochondria was tested in the presence of added succinate as a substrate. The effects of 100 uM heptachlor was tested in the presence of three kinds of substrates: succinate, beta-hydroxybutylate, and ascorbate plus N,N,N'N'-tetramethylphenylene-diamine. Heptachlor at 50 uM greatly inhibited the state 3 respiration, but inhibited the state 4 respiration hardly at all. The inhibition was released by 2,4-dinitrophenol. The higher dose suppressed state 3 and state 4 respiration almost completely with succinate as substrate. The findings suggest that the function of the electron transport system was also suppressed by the higher heptachlor dose even without oxidative phosphorylation.

Source: PubChem (NCBI) · compound 3589