Machado and Fanta [53] report that there were two effects of
methyl parathion: firstly, as a result of the direct contact of the
organophosphorus pesticides with the epithelial cells, including
those of the respiratory epithelium through which it entered the
organism; secondly after having been metabolized in the liver, by
distribution to the tissues through the blood flow in the form of
methyl parathion.
The results from cholinesterases activity assays prove the high
toxicity of methyl parathion to O. niloticus. P. mesopotamicus weighing
115 g exhibited high values of plasmatic ChEs inhibition (73%,
88% and 90% for AchE, PChE and BchE, respectively) when exposed
to 0.2 mg L1 of methyl parathion for 4 h [54], and B. cephalus
exposed to Folidol 600 exhibited 50–54% inhibition of plasmatic
ChEs [6]. These high values of inhibition for P. mesopotamicus and
B. cephalus, when compared to those obtained for O. niloticus, are
likely due to differences in body weight, species resistance,
absorption rate, detoxification and/or activation of the pesticide.
The effects of sublethal doses of methyl parathion on liver and
kidney morphology, as well as behavior of Callichthys callichthys included
alterations in the behavioral patterns of motility, feeding