title: Similarities and differences between the massive eel (Anguilla anguilla L.) devastations that occurred in Lake Balaton in 1991 and 1995.
abstract: In the past few years, two massive eel (Anguilla anguilla L.) devastations occurred in Lake Balaton, Hungary. In 1991, 300 tons of eel perished in the western basin of the lake, while in the summer of 1995 30 tons of eel died in the eastern part of the lake. Investigations carried out to find the causes of these ecocatastrophes included measurements of certain biochemical parameters: the blood sugar level, and the acetylcholinesterase (AChE, EC 3.1.1.7), lactate dehydrogenase (LDH, EC 1.1.2.3), glutamic-oxaloacetic transaminase (GOT, EC 2.6.1.1) and glutamic-pyruvic transaminase (GPT, EC 2.6.1.2) activities in the blood serum of the collected eels. In both 1991 and 1995, deltamethrin (DM), the active ingredient of the insecticide K-OTHRIN 1 ULV used against mosquitoes, was detected in the eels; in 1995 it was demonstrated in several other animal species, i.e., bream (Abramis brama L.), pike perch (Stizostedion lucioperca L.), and the common gull (Larus canus), and in sediment samples from the lake. Additionally, laboratory experiments were carried out to study the effects of DM on eels. In 1991, eels were collected from the western (the site of the devastation) and eastern basins of the lake. The eels from the eastern basin were used as controls. At that time, the AChE activity in the blood serum of the eels from the western basin was significantly inhibited compared to that in animals from the eastern basin (P < 0.05, Student t test). Eels from the western part of the lake had GOT and GPT levels 20 and 100%, respectively, higher than those of eels from the eastern part of the lake. The blood glucose level was much higher in the eels from the affected area of the lake as compared to those from the eastern part. The brain and liver of the eels contained DM residues at 20 micrograms/kg wet tissue (Gönczy, 1992). Gönczy suspected that one of the causes of the massive eel loss in 1991 was the presence of DM in the fish. In 1995, when the eel devastation occurred in the eastern basin, moribund and surviving eels were collected from this part of the lake. The AChE activity was significantly inhibited in the blood serum of the dying eels as compared to that in surviving animals (P < 0.05, Student t test). The blood glucose content exhibited a difference too: it was 2.5 times higher in the dying eels than in the surviving ones. A huge increase in the LDH level was measured in the dying eels, indicating damage to different muscle tissues to an extent never observed previously. The GOT activities of the serum were twice as high in the dying eels as in the living fish. The GPT was not significantly changed in the serum of dying eels as compared to the surviving animals. DM was detected in different tissue samples of the dying eels: 2.7-18.5 micrograms/kg in the liver, 9.0-31.1 micrograms/kg in the gill, and 3.0 micrograms/kg wet tissue in the muscle. DM residues were found in tissue samples from other animals, in the following concentrations: 0.4 micrograms/kg in bream, 2.1 micrograms/kg in pike perch, 1.1 micrograms/kg wet tissue in dead gulls. The sediment samples collected from different places and at different times contained DM in a concentration of 5.5-30.0 micrograms/kg wet sediment at the time of the eel deaths, while the sediment samples collected from the same places a month later still contained DM at 7.0-8.8 micrograms/kg wet sediment. Laboratory experiments with the insecticide K-OTHRIN 1 ULV revealed that 1.0 microgram/liter of its active ingredient, DM, caused the death of 50% of the eels after an incubation time of 96 hr. In the liver of the dead eels, DM was detected at 2.9-20.0 micrograms/kg wet tissue. All the above-mentioned changes and the DM residue detected in the eels appear to demonstrate the contribution of DM in the severe eel devastation. This finding on the ecological risk of such types of insecticides might be useful in their further application.
authors.affiliation: Bay Zoltán Foundation for Applied Research, Institute for Biotechnology, Szeged, Hungary.
authors.forename: T
authors.initials: T
authors.lastname: Bálint
authors.forename: J
authors.initials: J
authors.lastname: Ferenczy
authors.forename: F
authors.initials: F
authors.lastname: Kátai
authors.forename: I
authors.initials: I
authors.lastname: Kiss
authors.forename: L
authors.initials: L
authors.lastname: Kráczer
authors.forename: O
authors.initials: O
authors.lastname: Kufcsák
authors.forename: G
authors.initials: G
authors.lastname: Láng
authors.forename: C
authors.initials: C
authors.lastname: Polyhos
authors.forename: I
authors.initials: I
authors.lastname: Szabó
authors.forename: T
authors.initials: T
authors.lastname: Szegletes
authors.forename: J
authors.initials: J
authors.lastname: Nemcsók
mesh_terms: D000110:Acetylcholinesterase / Q000097:blood / Q000378:metabolism; D000410:Alanine Transaminase / Q000097:blood / Q000378:metabolism; D000811:Anguilla / Q000502:physiology*; D000818:Animals; D001219:Aspartate Aminotransferases / Q000097:blood / Q000378:metabolism; D001786:Blood Glucose / Q000378:metabolism; D002374:Catalase / Q000097:blood / Q000378:metabolism; D005393:Fish Diseases / Q000139:chemically induced* / Q000378:metabolism; D005399:Fishes / Q000378:metabolism; D006814:Hungary; D007306:Insecticides / Q000506:poisoning*; D007770:L-Lactate Dehydrogenase / Q000097:blood / Q000378:metabolism; D009570:Nitriles; D011722:Pyrethrins / Q000506:poisoning*; D014874:Water Pollutants, Chemical / Q000506:poisoning*
chemical_list: D001786:Blood Glucose; D007306:Insecticides; D009570:Nitriles; D011722:Pyrethrins; D014874:Water Pollutants, Chemical; C017180:decamethrin; D007770:L-Lactate Dehydrogenase; D002374:Catalase; D001219:Aspartate Aminotransferases; D000410:Alanine Transaminase; D000110:Acetylcholinesterase