Organophosphates inhibit catecholamine secretion and calcium influx in bovine adrenal chromaffin cells.
The lethality of organophosphorous compounds has been attributed to their inhibitory effect on acetylcholinesterase (AChE) in the nervous system. However, subacute exposure of humans to organophosphates induces cognitive and emotional defects which might not solely be attributable to AChE inhibition. Therefore we investigated the toxic effects of methyl parathion and malathion on bovine adrenal chromaffin cells. Catecholamine secretion and 45Ca2+ uptake evoked by either a nicotinic agonist (DMPP) or high [K+] were inhibited by methyl parathion and malathion. The [Ca2+]i rise induced by DMPP was inhibited by both compounds. We conclude that in addition to AChE, voltage-gated Ca2+ channels and nicotinic receptors are possible sites of action of organophosphates in mammalian systems.
Liu
P S
PS
Department of Microbiology, Soochow University, Shihlin, Taipei, Taiwan, ROC.
Kao
L S
LS
Lin
M K
MK
D000313:Adrenal Medulla / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000187:drug effects; D002417:Cattle; D002478:Cells, Cultured / Q000187:drug effects / Q000378:metabolism; D002837:Chromaffin Granules / Q000187:drug effects / Q000378:metabolism; D015640:Ion Channel Gating / Q000187:drug effects; D008294:Malathion / Q000633:toxicity*; D008743:Methyl Parathion / Q000633:toxicity*; D009638:Norepinephrine / Q000378:metabolism*; D011978:Receptors, Nicotinic / Q000187:drug effects / Q000378:metabolism
D015220:Calcium Channels; D011978:Receptors, Nicotinic; D008743:Methyl Parathion; D002118:Calcium; D008294:Malathion; D009638:Norepinephrine