Glycolysis and Krebs Cycle Metabolites in Mosquitofish, Gambusia Holbrooki, Girard 1859, Exposed to Mercuric Chloride: Allozyme Genotype Effects

Abstract

Concentrations of glycolysis and Krebs (citric acid) cycle metabolites were measured in the tail tissues of mosquitofish (Gambusra holbrooki, Girard 1859) in response to exposure to 0.86 mg/L Hg (as HgCI,) for 28 h. Substrate and product concentrations were compared between allozyme genotypes at two loci (glucosephosphate isomerase-2 and malate dehydrogenase-l) 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 G~1 -2~~'~~ exhibited an overall increase in glycolytic activity in response to mercury treatment.

Genetic and demographic responses of mosquitofish (Gambusia holbrooki) populations exposed to mercury for multiple generations

“…This indicated that the relationship at the Gpi‐2 locus was not toxicant specific. Differences in glycolytic and Krebs cycle metabolite concentrations were observed among Gpi‐2 genotypes during acute mercury exposures [15,16]. Glycolytic flux was highest in mos‐quitofish homozygous for the Gpi‐2 38 allele, suggesting inefficient use of metabolic resources in comparison to other Gpi‐2 genotypes [16].…”

Enhanced uranium tolerance of an exposed population of the eastern mosquitofish (Gambusia holbrooki Girard 1859)

“…Furthermore, a low frequency of the Gpi-238 allele in a population exposed to elevated mercury was consistent with predictions drawn from laboratory studies (Heagler et al 1993). Kramer et al (1992) reported that the Gpi-238/38 genotype had a distinct shift in glycolytic metabolites during mercury stress that may be associated with intolerance.…”

Mercury Hazards from Gold Mining to Humans, Plants, and Animals

“…Sublethal concentrations of mercury are known to adversely affect sensitive species of aquatic biota through inhibition of reproduction (Dave and Xiu 1991;Kanamadi and Saidapur 1991;Kirubagaran and Joy 1992;Khan and Weis 1993;Punzo 1993), reduction in growth rate (Kanamadi and Saidapur 1991;Punzo 1993), increased frequency of tissue histopathology Joy 1988, 1989;Handy and Penrice 1993;Voccia et al 1994), impairment in ability to capture prey (Weis and Weis 1995) and olfactory receptor function , alterations in blood chemistry (Allen 1994) and enzyme activities (Nicholls et al 1989;Kramer et al 1992), disruption of Birge et al 1979;2, USEPA 1985;3, Hudson et al 1984;4, Hill 1981;5, Hill and Soares 1984;6, Heinz and Locke 1976;7, Scheuhammer 1988;8, Spann et al 1972;9, Finley et al 1979;10, Hamasaki et al 1995;11, Khera 1979;12, Eaton et al 1980;13, Sheffy and St. Amant 1982;14, Kucera 1983;15, Ropek and Neely 1993;16, Ronald et al 1977. thyroid function (Kirubagaran and Joy 1989), chloride secretion (Silva et al 1992), and other biochemical and metabolic functions (Nicholls et al 1989;Angelow and Nicholls 1991). In general, the accumulation of mercury by aquatic biota is rapid and depuration is slow (Newman and Doubet 1989;Angelow and Nicholls 1991;Wright et al 1991;Handy and Penrice 1993;…”