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Glycolysis and krebs cycle metabolites in mosquitofish, Gambusia holbrooki , Girard 1859, exposed to mercuric chloride: Allozyme genotype effects
Author(s) -
Newman Michael C.,
Mulvey Margaret,
Kramer Vincent J.,
Ultsch Gordon R.
Publication year - 1992
Publication title -
environmental toxicology and chemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.1
H-Index - 171
eISSN - 1552-8618
pISSN - 0730-7268
DOI - 10.1002/etc.5620110309
Subject(s) - mosquitofish , gambusia , biology , citrate synthase , glycolysis , malate dehydrogenase , genotype , citric acid cycle , locus (genetics) , mercury (programming language) , genetics , biochemistry , metabolism , enzyme , gene , fishery , fish <actinopterygii> , computer science , programming language
Abstract Concentrations of glycolysis and Krebs (citric acid) cycle metabolites were measured in the tail tissues of mosquitofish (Gambusia holbrooki , Girard 1859) in response to exposure to 0.86 mg/L Hg (as HgCl 2 ) for 28 h. Substrate and product concentrations were compared between allozyme genotypes at two loci (glucosephosphate isomerase‐2 and malate dehydrogenase‐1) to determine whether allozyme genotypes in mosquitofish were differentially inhibited by mercury. Mercury treatment, regardless of allozyme genotype, caused decreased concentrations of glucose‐6‐phosphate (‐27%) and lactate (‐27%). Mercury treatment led to increased concentrations of malate (+33%) and oxaloacetate (+28%). Increased Krebs cycle activity could have been a response to greater energy needs associated with maintaining homeostasis under stressful conditions. There was no evidence of differential inhibition of allozymes at either locus. Fish of genotype Gpi ‐2 38/38 exhibited an overall increase in glycolytic activity in response to mercury treatment.