Document Detail

The effect of lead on the metabolic and energetic status of the Yabby, Cherax destructor, during environmental hypoxia.
MedLine Citation:
PMID:  16083977     Owner:  NLM     Status:  MEDLINE    
The concomitant effects of Pb and hypoxia on respiration and muscle energy status were examined in the freshwater crayfish Cherax destructor to determine if Pb intoxication exacerbated the effects of hypoxia. C. destructor, either intoxicated for 14 days with 0.5 mgL(-1)Pb, or from Pb-free control conditions, were subjected to progressive hypoxia at -2.7 kPah(-1) to a O2 partial pressure in the water (PwO2) of 1.33 kPa. This hypoxia was then sustained for 3 h. Pb-exposure reduced O2-uptake (MO2) at all PwO2 above 1.33 kPa but without any saving in ventilation, implying that Pb either unlinked ventilation from actual O2 requirements or rendered O2 transfer across the gill less efficient. Hypoxia alone induced no change in the adenylate energy charge (AEC), total adenylate (TAN), ATP/ADP ratio or in the equilibrium constant for adenylate kinase K'(ADEN), apparently due to protection of ATP levels by arginine phosphate. Under maximal hypoxia (PwO2=1.33 kPa) the Pb-exposed crayfish increased muscle ADP by 73% (tail) and 158% (chelae) but without any change in AMP, ATP or TAN. Thus, AEC declined (chelae AEC=0.71; tail AEC=0.85), as did the ATP/ADP ratio and K'(ADEN). L-Lactate increased in the muscle tissues of control but not Pb-exposed crayfish, consistent with a lowered O2 requirement in the Pb-exposed animals. The Pb intoxication slowed respiration and probably glycolysis, possibly altering the [ATP]:[ADP] equilibrium concentrations for adenylate kinase K'(AK). Lowered MO2 during severe hypoxia slows oxidative phosphorylation and ADP accumulation could occur as non-utilised substrate and may reflect a transient disequilibrium. During this time ATP levels were protected by arginine phosphate. AEC is sensitive to Pb in hypoxic crayfish but the changes have low importance for the energetic competence of the crayfish. During sustained hypoxia the crayfish recovered their energy status regardless of the Pb-exposure and this was, therefore, not a feature of Pb intoxication. Consequently, the ADP was recovered into the ATP pool of the hypoxic crayfish, and demand on arginine phosphate relieved. The Pb exposure did not otherwise exacerbate the effect of sustained hypoxia and C. destructor appeared to cope well with Pb intoxication, apparently by a specific Pb-induced hypometabolism separate from hypoxic response. Lowered metabolism as a survival response has limitations in the longer term and the implications for crustaceans generally warrant further study.
S Morris; W J van Aardt; M D Ahern
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Publication Detail:
Type:  Comparative Study; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Aquatic toxicology (Amsterdam, Netherlands)     Volume:  75     ISSN:  0166-445X     ISO Abbreviation:  Aquat. Toxicol.     Publication Date:  2005 Oct 
Date Detail:
Created Date:  2005-09-19     Completed Date:  2006-03-28     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8500246     Medline TA:  Aquat Toxicol     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  16-31     Citation Subset:  IM    
School of Biological Sciences, University of Bristol, Woodland Road, Bristol BS8 1UG, UK.
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MeSH Terms
Adenosine Diphosphate / metabolism
Adenosine Triphosphate / metabolism
Adenylate Kinase / metabolism
Analysis of Variance
Arginine / analogs & derivatives,  metabolism
Decapoda (Crustacea) / drug effects*,  metabolism*
Energy Metabolism / drug effects*
Lactic Acid / metabolism
Lead / toxicity*
Muscles / metabolism
Organophosphorus Compounds / metabolism
Oxygen / analysis*
Oxygen Consumption / drug effects
Seawater / chemistry
Reg. No./Substance:
0/Organophosphorus Compounds; 1189-11-3/phospho-L-arginine; 50-21-5/Lactic Acid; 56-65-5/Adenosine Triphosphate; 58-64-0/Adenosine Diphosphate; 74-79-3/Arginine; 7439-92-1/Lead; 7782-44-7/Oxygen; EC Kinase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

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