Toxicity of parathion on embryo and yolk-sac larvae of gilthead seabream (Sparus aurata l.): effects on survival, cholinesterase, and carboxylesterase activity.

This study was conducted to examine the acute toxicity of the organophosphorus pesticide (OP) parathion on embryos and yolk-sac larvae of gilthead seabream (Sparus aurata), and to investigate the effects of this compound on cholinesterase and carboxylesterase activity of seabream larvae in the phase of endogenous feeding. The 72-h LC50 for yolk-sac larvae (0.523 mg L⁻¹) was about two-fold lower than the 48-h LC50 for embryos (1.005 mg L⁻¹). Parathion significantly inhibited the activity of ChE and CaE activity in yolk sac larvae but there were not significant differences in the sensitivity of both esterases to parathion as inferred by their 72-h IC50 values. Larvae exposed to parathion for 72 h showed a 70% inhibition of the whole body acetylcholinesterase at approximately the LC50.

Toxicity of malathion at early life stages of the Senegalese sole, Solea senegalensis (Kaup, 1858): notochord and somatic disruptions.

The toxicity of malathion to Solea senegalensis was studied in a static renewal bioassay for 24, 48 and 72 h, with toxicant concentrations ranging from 1.56 until 100 µgL⁻¹. The LC50 values of malathion for 48 and 72 h was 63.5 (95% C.I: 50.83-79.34) and 22.94 (95% C.I: 17.16-30.68) µgL⁻¹ respectively. The survival of larvae was non-affected by exposure to malathion at concentrations up to 25 µgL⁻¹ (24 h NOEC), 6.25 µgL⁻¹ (48 h NOEC) and <1.6 µg⁻¹ (72 h NOEC). At the end of the experiment, surviving larvae from concentrations smaller than the 72h-LC50 were chosen to study morphological changes during malathion exposure. Results revealed a strong disruption in the notochord and trunk musculature integrity as a result of toxicant exposure. Noticeable changes in the composition and reduction of collagen fibers from the perinotochordal connective sheath and perimysium were clearly detected. The trunk musculature was also altered, showing a general disorganization of fibers. Moreover, malathion exposure provoked pericardial and yolk-sac oedemas and histopathological alterations in some other organ- systems and tissues (i.e. liver, pancreas, intestine).

Cholinesterase activity in gilthead seabream (Sparus aurata) larvae: Characterization and sensitivity to the organophosphate azinphosmethyl.

Assessment of cholinesterase (ChE) inhibition is widely used as a specific biomarker for evaluating the exposure and effects of non-target organisms to anticholinesterase agents. Cholinesterase and carboxylesterase activities have been measured in larvae of gilthead seabream, Sparus aurata, during the endogenous feeding stage, and ChE was characterized with the aid of diagnostic substrates and inhibitors. The results of the present study showed that whole-body ChE of yolk-sac seabream larvae possesses typical properties of acetylcholinesterase (AChE) with a apparent affinity constant (K(m)) of 0.163+/-0.008 mM and a maximum velocity (V(max)) of 332.7+/-2.8 nmol/min/mg protein. Moreover, sensibility of this enzyme was investigated using the organophosphorus insecticide azinphosmethyl. Static-renewal toxicity tests were conducted over 72 h and larval survival and AChE inhibition were recorded. Mean mortality of seabream larvae increased with increasing concentrations of azinphosmethyl and exposure duration. The estimated 72-h LC50 value to azinphosmethyl was 4.59 microg/l (95% CI=0.46-8.71 microg/l) and inhibition of ChE activity gave an IC50 of 3.04 microg/l (95% CI=2.73-3.31 microg/l). Larvae exposed to azinphosmethyl for 72h showed a 70% inhibition of the whole-body acetylcholinesterase activity at approximately the LC50. In conclusion, the results of the present study suggested that monitoring ChE activity is a valuable tool indicating OP exposure in S. aurata larvae and that acetylthiocholine is the most appropriate substrate for assessing ChE inhibition in this early-life stage of the fish.