Relationships between mercury body concentrations, standard metabolic rate, and body mass in eastern mosquitofish (Gambusia holbrooki) from three experimental populations

Abstract

Eastern mosquitofish (Gambusia holbrooki) were sampled from three experimental populations (two Hg-exposed populations and one reference population) to determine whether transgenerational exposure (lifelong exposure of multiple generations) to Hg adversely affects standard metabolic rate (SMR). Mosquitofish subjected to lifelong Hg exposure accumulated significant concentrations of Hg in their tissues compared to fish from the reference population (mean: 3.89-4.13 vs 0.08 microHg/g wet mass, respectively). Less than 10% of the variability in Hg tissue concentrations could be explained by fish body mass, likely because of the short life span and/or dietary habits of this species. Despite the high body burdens of Hg in exposed fish, we found no significant difference in SMR among individuals from Hg-exposed or reference populations. Our findings contrast recent laboratory work describing elevated SMR in mosquitofish exposed to 100 microg/L dissolved inorganic Hg for 48 h. To account for contrasting results between studies, we hypothesize that acute exposure to dissolved inorganic Hg damages gill epithelium, resulting in increased metabolic rate, but that lifelong Hg exposure via trophic uptake of methyl mercury does not affect fish respiratory structures. Alternative hypotheses include the possibility that G. holbrooki is a species that can tolerate high body burdens of Hg or that more than four years of genetic isolation during Hg exposure (8-12 generations) resulted in selection for Hg-tolerant or -resistant individuals.

Cardiorespiratory responses to graded hypoxia in the neotropical fish matrinxã (Brycon amazonicus) and traíra (Hoplias malabaricus) after waterborne or trophic exposure to inorganic mercury

“…Exposure to metals often disturbs normal metabolic processes in fish, including irritation of respiratory epithelium, changes in ventilation frequency, inefficient O 2 delivery to tissues, changes iṅ VO 2 , and increased energy requirements to resist or repair toxicantinduced damage (Hopkins et al, 2003). In the present study, HgCl 2 significantly increased the P c O 2 of B. amazonicus and H. malabaricus and these species became more susceptible and dependent of the environmental P in O 2 at higher tensions.…”

Mercury levels of small fishes: influence of size and catch area

“…The gap between mercury ingested and eliminated might cause mercury accumulation in fishes, resulting in the correlation between body size and mercury level. However, in small fishes that do not exhibit marked differences in size, size may only explain *10% of the observed variation in mercury levels [21]. As a result, such size relationships may not hold at very low mercury levels, as in the present study.…”

Acute Toxicity, Uptake and Histopathology of Aqueous Methyl Mercury to Fathead Minnow Embryos

“…Through all three of these uptake mechanisms, aqueous uptake, maternal transfer, and food-web bioamplification, fish can accumulate significant body burdens of mercury. Hopkins et al (2003) studied mercury concentrations in several generations of eastern mosquitofish, Gambusia holbrooki, in an experimental ecosystem with mercury concentrations in the water column of less than 50 ng/l. As a result of biomagnification of mercury in the aquatic food webs, body burdens of greater than 4.0 lg/g ww were reported in adult fish.…”

“…This study utilizes exposure concentrations of MeHg in the lg/l range which are several orders of magnitude higher than the ng/l range typically found in the natural environment (U.S. EPA, 2001). These naturally-occurring, low-levels of environmental MeHg are not necessarily indicative of mercury levels found in embryos due to its foodweb bioamplification and maternal transfer Latif et al, 2001;Hopkins et al, 2003). The current study was designed to examine a number of general toxicological endpoints including acute toxicity, bioaccumulation, total protein production, mitotic effects and pathology.…”