Ammonium is one of the final products following catabolism,
principally of amino acids that might have an alimentary or muscular
origin, depending on nutritional conditions [49]. In addition
to being used as energy substrates and components of body structures,
amino acids can be more important than ions in the maintenance
of osmotic pressure in prawns, such as P. setiferus [50,51].
Typically, increases in ammonium excretion reflect an increase in
catabolism of amino acids. However, when exposed to lethal concentrations
of methyl parathion, dysfunction of ammonium excretion
control follows gill damage. This probably indicates an initial
loss of the osmotic balance in the cells. The regression of the wrinkling
afterwards could mean that the epithelium was still able to
make some adjustments after an initial aggression. Nitrogen excreted
by fish suggested a reduction of free amino acids catabolism
and/or else a polypeptide synthesis increase. Another explanation
could be the toxicant effect on gill epithelium, causing a shift in
the nitrogen excretion. Mucus secretion over the gill chamber
could be provoked by endosulfan exposure as it was observed in
the freshwater prawn Macrobrachium malcolmsonii [52]. Subsequent
studies by Machado and Fanta [53] demonstrate pathological
changes in gill tissue of the freshwater fish Metynnis roosevelti
exposed to methyl parathion for 8 h. The effect of methyl parathion
on M. roosevelti branchial epithelium was quite drastic, including
structural changes of the gill lamellae organization, epithelial
detachment, necrosis, hyperplasia, loss of the microridges, and altered
cellular morphology.