Abstract

This study, carried out on the estuarine crab Chasmagnathus granulata, had two main objectives: (i) to correlate inhibition of the cholinesterase activity in the thoracic ganglia caused by a commercial formulation of methyl parathion (O,O-dimethyl- o-p-nitro-phenyl phosphorothionate) with crab mortality; and (ii) to investigate the methyl parathion bioactivation mechanisms. In crabs not pre-exposed to sesamol (3, 4-methylenedioxyphenol), in vivo cholinesterase inhibition showed a dose-related response (ID 50 = 0.36 mg · kg −1). However, it showed not to be a good tool to establish an effective dose since small amounts of inhibition were correlated to mortalities as high as 50%. Methyl parathion was more toxic to crabs not pre-exposed to sesamol (96 hr LD 50 = 0.21 mg · kg −1) than crabs pre-exposed to the MFO-inhibitor (96 hr LD 50 = 1.02 mg · kg −1). Pre-exposure to sesamol seems to prevent methyl parathion oxidation, and consequently, its toxicity since the cholinesterase inhibition in crabs pre-exposed to sesamol was lower than that observed in those not pre-exposed to sesamol. In accordance to the idea that the anticholinesterase property of methyl parathion is acquired only after its oxidation, a higher in vitro cholinesterase inhibition induced by chemically oxidized methyl parathion (IC 50 = 0.114 μM) in relation to that caused by the fresh methyl parathion (IC 50 = 19.2 μM) was observed.

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