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JOINT RESEARCH PROJECT ON THE AQUATIC ECOTOXICITY OF ORGANO-ALUMINIUM: ION REGULATION.

Ziel

THE OVERALL GOAL OF THE JOINT RESEARCH PROJECT IS TO RELATE THE TOXIC EFFECTS OF ALUMINIUM AND ITS ORGANO-COMPLEXES ON THE PHYSIOLOGY OF AQUATIC ORGANISMS TO THE UNDERLYING CHEMICAL AND PHYSIOLOGICAL PROCESSES INVOLVED, IN ORDER TO PREDICT THE IMPACT OF CHANGES IN THE ACIDIC FRESHWATER ENVIRONMENT ON THE BIOTA.

THIS PARTICULAR RESEARCH PROJECT INTENDS TO STUDY THE MECHANISMS OF THE TOXIC ACTION OF ORGANIC AND POLYMERIC AL IN ACID WATERS ON PHYSIOLOGICAL PROCESSES AS (1) THE NACL AND ACID-BASE RELATED ION TRANSFERS IN THE GILLS, (2) THE RESPIRATORY PROCESSES AND (3) THE HAEMATOLOGICAL PROCESSES IN FRESHWATER FISHES.
(1) THE TOXIC MECHANISMS OF ORGANIC AND POLYMERIC AL-COMPLEXES IN FISH.
TO FIND OUT WHETER ORGANIC AL-COMPLEXES EXCERT THEIR TOXIC ACTION AT THE EXTERNAL SIDE OF THE GILL EPITHELIUM (INCREASED NACL EFFLUX THROUGH PARACELLULAR PATHWAYS), OR WHETER THEY INTERFERE WITH NORMAL CELLULAR METABOLISM (INHIBITION OF ION UPTAKE, IMPAIRING GAS EXCHANGE), FOLLOWING EXPERIMENTS ARE PLANNED:
A) DIRECT INJECTION OF AL-COMPLEXES IN THE BLOOD OF THE FISH.
INTERNAL AL TOXICITY WILL BE STUDIED IN ACID EXPOSED FISH BY INTRAVENOUS INJECTION OF DIFFERENT AL-COMPLEXES. NACL IN- AND EFFLUXES WILL BE MEASURED IN THESE FISH, AND IN SHAM-INJECTED ACID-EXPOSED FISH. THE RETENTION OF AL AND ITS SPECIATION IN THE FISH WILL BE FOLLOWED: URINARY EXCRETION, ACCUMULATION IN SPECIFIC ORGANS (LIVER, BRAINS, BONES, GILLS) AND COMPLEXATION WITH METABOLITES. THESE RESULTS WILL BE EVALUATED IN REGARD WITH DATA ON EXTERNAL AL-EXPOSURE.
MAKING USE OF THE AL INJECTION METHODOLOGY, THE INTERACTION OF AL IN THE BODY WITH OSMOREGULATORY-RELATED BIOCHEMICAL PROCESSES AS NA-K ATPASE AND WITH RESPIRATION METABOLITES (HEME SYNTHESIS AND FERROXIDASE ACTIVITY) WILL BE STUDIED.

B) SUBCELLULAR LOCALISATION OF AL IN THE GILL EPITHELIUM.
TO LOCALISE AL IN THE GILL EPITHELIUM AT THE SUBCELLULAR LEVEL USING LAMMA (LASER MICROPROBE MASS ANALYSIS) IS A UNIQUE METHODOLOGY ESPECIALLY BECAUSE SUBCELLULAR LOCALISATION VIA CONVENTIAL METHODS (E.G. ULTRACENTRIFUGATION) IS IMPOSSIBLE DUE TO THE (COMMERCIALLY) UNAVAILABILITY OF AN AL TRACER. DATA ON THE SUBCELLULAR LOCALISATION OF AL MAY POINT DIRECTLY TO THOSE CELLULAR MECHANISMS WHICH ARE IMPAIRED BY THE AL.

(2) AMELIORATING EFFECT OF ORGANICALLY COMPLEXED AL ON ION LOSS.
IT HAS BEEN STATED THAT AL (AS AL+++) EXCERTS A PROTECTIVE ACTION TOWARDS ACID STRESS (E.G. DIMINISHED ION LOSSES), WHICH SEEMS TO BE COMPARABLE TO THE MODERATING ACTION OF CA++ IN RE-CLOSING THE PARACELLULAR CHANNELS IN FISH GILL EPITHELIA. SINCE THIS HYPOTHESIS IMPLIES THE PRESENCE OF IONIC AL+++ AS THE DOMINANT FORM, IT MAY NOT BE FULFILLED IN HUMIC RICH ACID WATERS. THIS QUESTIONABLE AMELIORATING ROLE OF ORGANICALLY COMPLEXED AL WILL BE TESTED BY MEASUREMENTS OF NACL IN- AND EFFLUXES IN WATER WITH AND WITHOUT HUMIC MATERIAL AT PH 4.5 OR LESS.

(3) ACCLIMATION, SENSITISATION AND RECOVERY OF PHYSIOLOGICAL PROCESSES.

LONGTERM EXPERIMENTS ARE PLANNED WHICH INTEND TO FIND OUT IF FISHES ARE ABLE TO DEVELOP PHYSIOLOGICAL COMPENSATORY MECHANISMS TO CHRONIC AL/ACID STRESS (ACCLIMATION) OR TO RE-ESTABLISH PRE-STRESS PHYSIOLOGICAL CONDITIONS (RECOVERY). SENSITISATION EXPERIMENTS ARE DESIGNED TO EVALUATE HOW THE ANIMALS REACT TO A SECOND STRESS (E.G. ORGANIC AL) AFTER A MILD ACID-STRESS PERIOD, AS DURING STRESS-EPISODES IN NATURAL WATERS. THESE EXPERIMENTS WILL BE PERFORMED WITH ACID-TOLERANT AND -SENSITIVE SPECIES (CATFISH AND TROUT), AS A CONTRIBUTIION TO OUR UNDERSTANDING OF THE FUNDAMENTAL MECHANISMS THAT ARE RESPONSIBLE FOR THE OBSERVED DIFFERENCES IN SENSITIVITY OF THE ION-REGULATORY MECHANISMS IN THESE SPECIES.

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CSC - Cost-sharing contracts

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BELGIAN NUCLEAR RESEARCH CENTRE
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Letzte Aktualisierung: 23 Januar 1994

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Permalink: https://cordis.europa.eu/project/id/EV4V0116/de

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